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1. Schiffmann SN: [Changes in neural networks by conditional transgenic approach: a key to our comprehension of neuro-psychiatric disorders in the basal ganglia system]. Bull Mem Acad R Med Belg; 2009;164(7-9):171-8; discussion 178-80
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  • [Title] [Changes in neural networks by conditional transgenic approach: a key to our comprehension of neuro-psychiatric disorders in the basal ganglia system].
  • The striatum, the first relay of the basal ganglia system, is critically involved in motor functions and motivational processes.
  • The striatum consists of two populations of neurons projecting at the origin of two distinct paths in the circuit of basal ganglia, and of different populations of interneurons.
  • To identify these specific functions, we have developed new animal models wearing molecular or cell "lesions" by a conditional transgenic approach to target a specific population of neurons.
  • By this approach, we demonstrated the inhibitory role of the population of striatopallidal neurons in the motor control and in the process of drug addiction, identified new genes selectively expressed by striatopallidal neurons that could be the target for future therapies and identified the potential role of this population of neurons disturbances in attention-deficit hyperactivity disorder (ADHD).
  • [MeSH-major] Basal Ganglia / physiopathology. Mental Disorders / physiopathology. Nerve Net / physiopathology. Nervous System Diseases / physiopathology
  • [MeSH-minor] Animals. Attention Deficit Disorder with Hyperactivity / physiopathology. Corpus Striatum / physiopathology. Humans. Huntington Disease / physiopathology. Mice. Mice, Knockout. Models, Animal. Movement Disorders / physiopathology. Neural Pathways / physiopathology. Neurons, Efferent / metabolism. Neuropeptides / metabolism. Nucleus Accumbens / physiopathology. Parkinson Disease / physiopathology. Rats. Rats, Transgenic. Receptors, Dopamine / metabolism. Substance-Related Disorders / physiopathology

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  • (PMID = 20218186.001).
  • [ISSN] 0377-8231
  • [Journal-full-title] Bulletin et mémoires de l'Académie royale de médecine de Belgique
  • [ISO-abbreviation] Bull. Mem. Acad. R. Med. Belg.
  • [Language] fre
  • [Publication-type] English Abstract; Lectures
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / Receptors, Dopamine
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2. Zhou M, Rebholz H, Brocia C, Warner-Schmidt JL, Fienberg AA, Nairn AC, Greengard P, Flajolet M: Forebrain overexpression of CK1delta leads to down-regulation of dopamine receptors and altered locomotor activity reminiscent of ADHD. Proc Natl Acad Sci U S A; 2010 Mar 2;107(9):4401-6
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  • Dopamine neurotransmission controls motor and perseverative behavior, is mediated by protein phosphorylation, and may be perturbed in disorders of attention and hyperactivity.
  • Under basal conditions, CK1delta OE mice exhibited horizontal and vertical hyperactivity, reduced anxiety, and nesting behavior deficiencies.
  • All together, under basal conditions and in response to drug stimulation, the behavioral phenotype of CK1delta OE mice is reminiscent of the symptoms and drug responses observed in attention-deficit/hyperactivity disorder and therefore the CK1delta OE mice appear to be a model for this disorder.

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  • (PMID = 20145109.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / P01 DA010044; United States / NIMH NIH HHS / MH / P01 MH040899; United States / NIDA NIH HHS / DA / DA10044
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Antagonists; 0 / Receptors, Dopamine D1; 0 / Receptors, Dopamine D2; 207ZZ9QZ49 / Methylphenidate; 6LR8C1B66Q / Dizocilpine Maleate; CK833KGX7E / Amphetamine; EC 2.7.11.1 / Casein Kinase Idelta
  • [Other-IDs] NLM/ PMC2840146
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3. Coulaud J, Durant S, Homo-Delarche F: Glucose homeostasis in pre-diabetic NOD and lymphocyte-deficient NOD/SCID mice during gestation. Rev Diabet Stud; 2010;7(1):36-46
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  • AIMS: Given that beta-cell stimulation is a natural feature of gestation, we hypothesized that glucose homeostasis is disturbed in gestate pre-diabetic NOD and non-diabetic NOD/SCID mice, which may accelerate the onset of diabetes and increase diabetes prevalence.
  • METHODS: During gestation and postpartum, mice were analyzed under basal feed conditions followed by glucose injection (1 g/kg, i.p.) after overnight fast, using glucose tolerance test (GTT).
  • RESULTS: 1. Basal glucagonemia rose markedly in first-gestation fed NOD mice.
  • 2. beta-cell hyperactivity was present earlier in first-gestation non-diabetic fasted NOD and NOD/SCID mice than in age-matched C57BL/6 mice, assessed by increased insulin/glucose ratio after GTT.
  • CONCLUSIONS: First-gestation pre-diabetic NOD and non-diabetic NOD/SCID mice exhibited beta-cell hyperactivity and deregulation of glucagon and/or corticosterone secretion.

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  • (PMID = 20703437.001).
  • [ISSN] 1614-0575
  • [Journal-full-title] The review of diabetic studies : RDS
  • [ISO-abbreviation] Rev Diabet Stud
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 9007-92-5 / Glucagon; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ PMC2923379
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4. Rommelfanger KS, Wichmann T: Extrastriatal dopaminergic circuits of the Basal Ganglia. Front Neuroanat; 2010;4:139
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  • [Title] Extrastriatal dopaminergic circuits of the Basal Ganglia.
  • The basal ganglia are comprised of the striatum, the external and internal segment of the globus pallidus (GPe and GPi, respectively), the subthalamic nucleus (STN), and the substantia nigra pars compacta and reticulata (SNc and SNr, respectively).
  • Dopamine has long been identified as an important modulator of basal ganglia function in the striatum, and disturbances of striatal dopaminergic transmission have been implicated in diseases such as Parkinson's disease (PD), addiction and attention deficit hyperactivity disorder.
  • However, recent evidence suggests that dopamine may also modulate basal ganglia function at sites outside of the striatum, and that changes in dopaminergic transmission at these sites may contribute to the symptoms of PD and other neuropsychiatric disorders.
  • Further insights into the dopaminergic modulation of basal ganglia function at extrastriatal sites may provide us with opportunities to develop new and more specific strategies for treating disorders of basal ganglia dysfunction.

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  • (PMID = 21103009.001).
  • [ISSN] 1662-5129
  • [Journal-full-title] Frontiers in neuroanatomy
  • [ISO-abbreviation] Front Neuroanat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC2987554
  • [Keywords] NOTNLM ; GABA / Parkinson's disease / basal ganglia / dopamine / globus pallidus / glutamate / substantia nigra / subthalamic nucleus
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5. Windels F, Carcenac C, Poupard A, Savasta M: Pallidal origin of GABA release within the substantia nigra pars reticulata during high-frequency stimulation of the subthalamic nucleus. J Neurosci; 2005 May 18;25(20):5079-86
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  • Basal levels of Glu and GABA in the GP and SNr were significantly higher in hemiparkinsonian than in intact rats.
  • These results provide neurochemical confirmation of the hyperactivity of the STN after dopaminergic denervation and suggest that the therapeutic effects of HFS-STN may result partly from the stimulation of pallidonigral fibers, thereby revealing a potential role for pallidal GABA in the inhibition of basal ganglial output structures during HFS-STN.
  • [MeSH-minor] Animals. Cell Count / methods. Chromatography, High Pressure Liquid / methods. Dose-Response Relationship, Radiation. Electrochemistry / methods. Electrodes. Functional Laterality. Glutamic Acid / metabolism. Immunohistochemistry / methods. Male. Microdialysis / methods. Oxidopamine / toxicity. Rats. Rats, Sprague-Dawley. Tyrosine 3-Monooxygenase / metabolism

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  • (PMID = 15901790.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3KX376GY7L / Glutamic Acid; 56-12-2 / gamma-Aminobutyric Acid; 8HW4YBZ748 / Oxidopamine; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
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6. Takeuchi Y: [Neurotransmission in developmental disorders]. No To Hattatsu; 2008 Nov;40(6):451-5
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  • Attention deficit/hyperactivity disorder (AD/HD) is a heterogeneous developmental disorder with an etiology that is not fully understood.
  • The neurotransmission of dopamine in subcortical regions such as the basal ganglia and limbic areas is synaptic; on the other hand, dopamine neurotransmission in the frontal cortex is quite different, because there are very few dopamine transporters (DAT) in the frontal cortex that allow dopamine to diffuse away from the dopamine synapse ("volume transmission").
  • Furthermore, serotonergic neurons exert an inhibitory effect on midbrain dopamine cell bodies, and they have an influence on dopamine release in terminal regions.
  • In addition to abnormal circuitry in specific limbic and neocortical areas of the cerebral cortex, impairments in brainstem, cerebellar, thalamic, and basal ganglia connections have been reported.
  • The first is cell migration, the second is unbalanced excitatory-inhibitory networks, and the third is synapse formation and pruning, the key factors being reelin, neurexin, and neuroligin.
  • [MeSH-major] Attention Deficit Disorder with Hyperactivity / physiopathology. Autistic Disorder / physiopathology. Dopamine / physiology. Neurons / physiology. Synaptic Transmission
  • [MeSH-minor] Animals. Brain / physiology. Cell Adhesion Molecules, Neuronal. Glutamic Acid / physiology. Humans. Membrane Proteins / physiology. Nerve Tissue Proteins / physiology. Norepinephrine / physiology. Serotonin / physiology

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  • (PMID = 19039985.001).
  • [ISSN] 0029-0831
  • [Journal-full-title] No to hattatsu. Brain and development
  • [ISO-abbreviation] No To Hattatsu
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules, Neuronal; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / neuroligin 3; 333DO1RDJY / Serotonin; 3KX376GY7L / Glutamic Acid; VTD58H1Z2X / Dopamine; X4W3ENH1CV / Norepinephrine
  • [Number-of-references] 20
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7. Morgan D, Gordon MN: Amyloid, hyperactivity, and metabolism: theoretical comment on Vloeberghs et al. (2008). Behav Neurosci; 2008 Jun;122(3):730-2
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  • [Title] Amyloid, hyperactivity, and metabolism: theoretical comment on Vloeberghs et al. (2008).
  • Potential explanations include increased locomotor activity or increased basal metabolism.

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  • [Copyright] (Copyright) 2008 APA, all rights reserved.
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  • (PMID = 18513144.001).
  • [ISSN] 0735-7044
  • [Journal-full-title] Behavioral neuroscience
  • [ISO-abbreviation] Behav. Neurosci.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG018478-09; United States / NINDS NIH HHS / NS / NS48335; United States / NIA NIH HHS / AG / AG18478; United States / NIA NIH HHS / AG / AG15490; United States / NIA NIH HHS / AG / AG25509; United States / NIA NIH HHS / AG / AG 04418,; United States / NIA NIH HHS / AG / R01 AG025509-04; United States / NIA NIH HHS / AG / R01 AG018478-09; United States / NIA NIH HHS / AG / P01 AG004418-250018; United States / NIA NIH HHS / AG / R01 AG025509; United States / NIA NIH HHS / AG / R01 AG018478; United States / NINDS NIH HHS / NS / R01 NS048335; United States / NIA NIH HHS / AG / P01 AG004418; United States / NIA NIH HHS / AG / AG25711; United States / NIA NIH HHS / AG / AG025509-04; United States / NIA NIH HHS / AG / P50 AG025711; United States / NIA NIH HHS / AG / R01 AG015490; United States / NIA NIH HHS / AG / AG004418-250018
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid
  • [Other-IDs] NLM/ NIHMS116685; NLM/ PMC2706527
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8. O'Mahony A, Raber J, Montano M, Foehr E, Han V, Lu SM, Kwon H, LeFevour A, Chakraborty-Sett S, Greene WC: NF-kappaB/Rel regulates inhibitory and excitatory neuronal function and synaptic plasticity. Mol Cell Biol; 2006 Oct;26(19):7283-98
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  • IkappaBalpha-SR expression also results in diminished basal GluR1 levels and impaired synaptic strength (input/output function), both of which are fully restored following activity-based task learning.
  • Consistent with diminished GAD65-derived inhibitory tone and enhanced excitatory firing, IkappaBalpha-SR+ mice exhibit increased late-phase long-term potentiation, hyperactivity, seizures, increased exploratory activity, and enhanced spatial learning and memory.

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  • (PMID = 16980629.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / C06 RR018928; United States / NIA NIH HHS / AG / R01 AG020904; United States / NIA NIH HHS / AG / AG 20904
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / Isoenzymes; 0 / RNA, Messenger; 0 / Receptors, AMPA; 0 / Transcription Factor RelA; 0 / glutamate receptor ionotropic, AMPA 1; 139874-52-5 / NF-kappaB inhibitor alpha; 3KX376GY7L / Glutamic Acid; 56-12-2 / gamma-Aminobutyric Acid; EC 4.1.1.15 / Glutamate Decarboxylase; EC 4.1.1.15 / glutamate decarboxylase 2
  • [Other-IDs] NLM/ PMC1592877
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9. Xu ZZ, Zhang L, Liu T, Park JY, Berta T, Yang R, Serhan CN, Ji RR: Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med; 2010 May;16(5):592-7, 1p following 597
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  • Here we report that peripheral (intraplantar) or spinal (intrathecal) administration of RvE1 or RvD1 in mice potently reduces inflammatory pain behaviors induced by intraplantar injection of formalin, carrageenan or complete Freund's adjuvant (CFA), without affecting basal pain perception.
  • RvE1 also abolishes transient receptor potential vanilloid subtype-1 (TRPV1)- and TNF-alpha-induced excitatory postsynaptic current increases and TNF-alpha-evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity in spinal dorsal horn neurons via inhibition of the extracellular signal-regulated kinase (ERK) signaling pathway.

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  • (PMID = 20383154.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK074448; United States / NIDCR NIH HHS / DE / DE019938-01; United States / NINDS NIH HHS / NS / R01 NS054932-03; United States / NINDS NIH HHS / NS / R01 NS054932; United States / NINDS NIH HHS / NS / NS054932-03; United States / NINDS NIH HHS / NS / NS067686-01; United States / NINDS NIH HHS / NS / NS67686; United States / NIDCR NIH HHS / DE / R01-DE17794; United States / NIGMS NIH HHS / GM / R01 GM038765; United States / NINDS NIH HHS / NS / F30 NS054362; United States / NIDDK NIH HHS / DK / R01 DK074448-05; United States / NIDCR NIH HHS / DE / DE017794-04; United States / NIDCR NIH HHS / DE / R01 DE017794; United States / NIGMS NIH HHS / GM / GM038765-23; United States / NIDCR NIH HHS / DE / R01 DE019938-01; United States / NINDS NIH HHS / NS / R01 NS054932-04; United States / NIGMS NIH HHS / GM / R37 GM038765-23; United States / NINDS NIH HHS / NS / R01 NS067686; United States / NIDDK NIH HHS / DK / DK074448-05; United States / NIDCR NIH HHS / DE / R01 DE017794-04; United States / NIGMS NIH HHS / GM / R37 GM038765; United States / NIDCR NIH HHS / DE / R01-DE019938; United States / NINDS NIH HHS / NS / R01-NS54362; United States / NINDS NIH HHS / NS / R01 NS067686-01; United States / NIDCR NIH HHS / DE / R01 DE019938; United States / NIGMS NIH HHS / GM / R37 GM38765; United States / NIDDK NIH HHS / DK / R01-DK074448
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid; 0 / Analgesics; 0 / resolvin D1; 25167-62-8 / Docosahexaenoic Acids; AAN7QOV9EA / Eicosapentaenoic Acid
  • [Other-IDs] NLM/ NIHMS196352; NLM/ PMC2866054
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10. Briot A, Deraison C, Lacroix M, Bonnart C, Robin A, Besson C, Dubus P, Hovnanian A: Kallikrein 5 induces atopic dermatitis-like lesions through PAR2-mediated thymic stromal lymphopoietin expression in Netherton syndrome. J Exp Med; 2009 May 11;206(5):1135-47
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  • Lack of LEKTI causes stratum corneum detachment secondary to epidermal proteases hyperactivity.
  • This proinflammatory and proallergic pathway is independent of the primary epithelial failure and is activated under basal conditions in NS keratinocytes.
  • This cell-autonomous process is already established in the epidermis of Spink5(-/-) embryos, and the resulting proinflammatory microenvironment leads to eosinophilic and mast cell infiltration in a skin graft model in nude mice.



11. Borchhardt KA, Hörl WH, Sunder-Plassmann G: Reversibility of 'secondary hypercalcitoninemia' after kidney transplantation. Am J Transplant; 2005 Jul;5(7):1757-63
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  • We examined the effect of kidney transplantation on basal and pentagastrin-stimulated CT in CKD patients with elevated screening CT levels.
  • Before transplantation, the median basal CT concentration of 17 patients was 31 pg/mL (13-76), and decreased to 8 pg/mL (4-28) at 23 months (2-34) after kidney transplantation (p < 0.00005).
  • Therefore, the increase of CT concentration in patients with impaired kidney function presumably reflects 'secondary hypercalcitoninemia' due to C-cell hyperactivity.

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  • (PMID = 15943636.001).
  • [ISSN] 1600-6135
  • [Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
  • [ISO-abbreviation] Am. J. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 9007-12-9 / Calcitonin; AYI8EX34EU / Creatinine; EF0NX91490 / Pentagastrin
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12. Zhou L, Gall D, Qu Y, Prigogine C, Cheron G, Tissir F, Schiffmann SN, Goffinet AM: Maturation of "neocortex isole" in vivo in mice. J Neurosci; 2010 Jun 9;30(23):7928-39
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  • Here, we show that Celsr3|Dlx mutant mice have no extrinsic neocortical connections yet survive to postnatal day 20, acquire a basic behavioral repertoire, and display spontaneous hyperactivity, with abnormal light/dark activity cycling.
  • Deep layer neurons were reduced in number, and their apical and basal dendritic arbors were blunted, with reduced synapse density.
  • [MeSH-minor] Animals. Cadherins / genetics. Cadherins / metabolism. Electrophysiology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Immunohistochemistry. In Situ Hybridization. Interneurons / physiology. Locomotion / physiology. Mice. Mice, Transgenic. Mutation. Patch-Clamp Techniques. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 20534841.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Celsr3 protein, mouse; 0 / Distal-less homeobox proteins; 0 / Homeodomain Proteins; 0 / Receptors, Cell Surface; 0 / Transcription Factors
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13. Zhang J, Guan Z: Pathways involved in somatosensory electrical modulation of dorsal cochlear nucleus activity. Brain Res; 2007 Dec 12;1184:121-31
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  • Our recent study has shown that somatosensory electrical stimulation may be useful to modulate sound-induced hyperactivity in the dorsal cochlear nucleus (DCN), a neural correlate of certain forms of tinnitus.
  • To address this issue, we conducted c-fos immunocytochemistry using hamsters and mapped neural activation in both auditory and non-auditory structures following transcutaneous electrical stimulation of the basal part of the pinna.
  • [MeSH-minor] Animals. Cell Count / methods. Cricetinae. Electric Stimulation / methods. Male. Mesocricetus. Neurons / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Stilbamidines / metabolism. Trigeminal Nuclei / metabolism. Trigeminal Nuclei / radiation effects. Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate / metabolism

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  • (PMID = 17964553.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; 0 / Proto-Oncogene Proteins c-fos; 0 / Stilbamidines; 0 / Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate
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14. Hirano M, Rakwal R, Shibato J, Sawa H, Nagashima K, Ogawa Y, Yoshida Y, Iwahashi H, Niki E, Masuo Y: Proteomics- and transcriptomics-based screening of differentially expressed proteins and genes in brain of Wig rat: a model for attention deficit hyperactivity disorder (ADHD) research. J Proteome Res; 2008 Jun;7(6):2471-89
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  • [Title] Proteomics- and transcriptomics-based screening of differentially expressed proteins and genes in brain of Wig rat: a model for attention deficit hyperactivity disorder (ADHD) research.
  • Two global omics approaches were applied to develop an inventory of differentially expressed proteins and genes in Wig rat, a promising animal model of attention-deficit hyperactivity disorder (ADHD).
  • Peptide mass fingerprinting/tandem mass spectrometry identified 19 nonredundant proteins, belonging to 7 functional categories, namely, signal transduction, energy metabolism, cellular transport, protein with binding function, protein synthesis, cytoskeleton, and cell rescue.
  • [MeSH-minor] Animals. Attention Deficit Disorder with Hyperactivity / genetics. Attention Deficit Disorder with Hyperactivity / metabolism. Attention Deficit Disorder with Hyperactivity / pathology. Basal Ganglia / metabolism. Disease Models, Animal. Electrophoresis, Gel, Two-Dimensional. Frontal Lobe / metabolism. Male. Mesencephalon / metabolism. Oligonucleotide Array Sequence Analysis. Rats. Rats, Inbred LEC. Rats, Mutant Strains. Rats, Wistar. Spectrometry, Mass, Electrospray Ionization. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Tandem Mass Spectrometry

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  • (PMID = 18457438.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins
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15. Szucs RP, Frankel PS, McMahon LR, Cunningham KA: Relationship of cocaine-induced c-Fos expression to behaviors and the role of serotonin 5-HT2A receptors in cocaine-induced c-Fos expression. Behav Neurosci; 2005 Oct;119(5):1173-83
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  • Significant correlations were observed between cocaine-induced hyperactivity and c-Fos expression in the nucleus accumbens core (NAcC), caudate-putamen (CPu), and subthalamic nucleus.
  • [MeSH-minor] Analysis of Variance. Animals. Basal Ganglia / drug effects. Basal Ganglia / metabolism. Cell Count / methods. Dose-Response Relationship, Drug. Drug Interactions. Fluorobenzenes / pharmacology. Immunohistochemistry / methods. Male. Motor Activity / drug effects. Piperidines / pharmacology. Rats. Rats, Sprague-Dawley. Serotonin Antagonists / pharmacology

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  • (PMID = 16300424.001).
  • [ISSN] 0735-7044
  • [Journal-full-title] Behavioral neuroscience
  • [ISO-abbreviation] Behav. Neurosci.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA 00260; United States / NIDA NIH HHS / DA / DA 06057; United States / NIDA NIH HHS / DA / DA 06511; United States / NIDA NIH HHS / DA / DA 07287; United States / NIDA NIH HHS / DA / DA06059
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Uptake Inhibitors; 0 / Fluorobenzenes; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-fos; 0 / Receptor, Serotonin, 5-HT2A; 0 / Serotonin Antagonists; 139290-65-6 / MDL 100907; I5Y540LHVR / Cocaine
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16. Pertaya N, Marshall CB, Celik Y, Davies PL, Braslavsky I: Direct visualization of spruce budworm antifreeze protein interacting with ice crystals: basal plane affinity confers hyperactivity. Biophys J; 2008 Jul;95(1):333-41
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  • [Title] Direct visualization of spruce budworm antifreeze protein interacting with ice crystals: basal plane affinity confers hyperactivity.
  • It has been proposed that the exceptional activity of these AFPs depends on their ability to prevent ice growth at the basal plane.
  • To test the hypothesis that the hyperactivity of sbwAFP results from direct affinity to the basal plane, we fluorescently tagged sbwAFP and visualized it on the surface of ice crystals using fluorescence microscopy.
  • SbwAFP accumulated at the six prism plane corners and the two basal planes of hexagonal ice crystals.
  • In contrast, fluorescently tagged fish type III AFP did not adhere to the basal planes of a single-crystal ice hemisphere.
  • When ice crystals were grown in the presence of a mixture of type III AFP and sbwAFP, a hybrid crystal shape was produced with sbwAFP bound to the basal planes of truncated bipyramidal crystals.
  • These observations are consistent with the blockage of c-axial growth of ice as a result of direct interaction of sbwAFP with the basal planes.

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  • (PMID = 18339740.001).
  • [ISSN] 1542-0086
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifreeze Proteins; 0 / Ice
  • [Other-IDs] NLM/ PMC2426666
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17. Steiner MA, Marsicano G, Nestler EJ, Holsboer F, Lutz B, Wotjak CT: Antidepressant-like behavioral effects of impaired cannabinoid receptor type 1 signaling coincide with exaggerated corticosterone secretion in mice. Psychoneuroendocrinology; 2008 Jan;33(1):54-67
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  • Hypothalamic-pituitary-adrenocortical (HPA) axis hyperactivity is associated with major depressive disorders, and treatment with classical antidepressants ameliorates not only psychopathological symptoms, but also the dysregulation of the HPA axis.
  • We demonstrate that the genetic inactivation of CB1 is accompanied by increased plasma corticosterone levels both under basal conditions and at different time points following exposure to the FST.

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  • (PMID = 17976922.001).
  • [ISSN] 0306-4530
  • [Journal-full-title] Psychoneuroendocrinology
  • [ISO-abbreviation] Psychoneuroendocrinology
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / MH066172-01; United States / NIMH NIH HHS / MH / P50 MH066172; United States / NIMH NIH HHS / MH / P50 MH066172-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antidepressive Agents, Tricyclic; 0 / Piperidines; 0 / Pyrazoles; 0 / Receptor, Cannabinoid, CB1; 158681-13-1 / rimonabant; TG537D343B / Desipramine; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ NIHMS38680; NLM/ PMC2267923
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18. Marcellino D, Carriba P, Filip M, Borgkvist A, Frankowska M, Bellido I, Tanganelli S, Müller CE, Fisone G, Lluis C, Agnati LF, Franco R, Fuxe K: Antagonistic cannabinoid CB1/dopamine D2 receptor interactions in striatal CB1/D2 heteromers. A combined neurochemical and behavioral analysis. Neuropharmacology; 2008 Apr;54(5):815-23
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  • Antagonistic CB(1)/D(2) interactions were also discovered at the behavioral level through an analysis of quinpirole-induced locomotor hyperactivity in rats.
  • The CB(1) receptor agonist CP 55,940 at a dose that did not change basal locomotion was able to block quinpirole-induced increases in locomotor activity.
  • [MeSH-minor] Animals. Behavior, Animal. Cell Line, Transformed. Cyclohexanols / pharmacology. Dopamine / pharmacology. Dopamine Agonists. Drug Interactions. Fluorescence Resonance Energy Transfer / methods. Guanylyl Imidodiphosphate / pharmacology. Humans. Luminescent Proteins / metabolism. Male. Protein Binding / drug effects. Quinpirole / pharmacology. Radiography. Rats. Rats, Sprague-Dawley. Rats, Wistar. Receptors, Cannabinoid / metabolism. Transfection / methods

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  • (PMID = 18262573.001).
  • [ISSN] 0028-3908
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclohexanols; 0 / Dopamine Agonists; 0 / Dopamine D2 Receptor Antagonists; 0 / Luminescent Proteins; 0 / Receptor, Cannabinoid, CB1; 0 / Receptors, Cannabinoid; 0 / Receptors, Dopamine D2; 20OP60125T / Quinpirole; 34273-04-6 / Guanylyl Imidodiphosphate; 83003-12-7 / 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol; VTD58H1Z2X / Dopamine
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19. Surucu B, Bozulic L, Hynx D, Parcellier A, Hemmings BA: In vivo analysis of protein kinase B (PKB)/Akt regulation in DNA-PKcs-null mice reveals a role for PKB/Akt in DNA damage response and tumorigenesis. J Biol Chem; 2008 Oct 31;283(44):30025-33
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  • To address this, we analyzed basal, insulin-induced, and DNA damage-induced PKB Ser-473 phosphorylation in DNA-PK catalytic subunit-null DNA-PKcs(-/-) mice.
  • Moreover, DNA-PKcs(-/-) mice showed a tissue-specific increase in basal PKB phosphorylation.
  • In particular, persistent PKB hyperactivity in the thymus apparently contributed to spontaneous lymphomagenesis in DNA-PKcs(-/-) mice.



20. Wong CK, Wong PT, Tam LS, Li EK, Chen DP, Lam CW: Activation profile of intracellular mitogen-activated protein kinases in peripheral lymphocytes of patients with systemic lupus erythematosus. J Clin Immunol; 2009 Nov;29(6):738-46
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  • RESULTS AND DISCUSSION: The basal expressions of phospho-p38 MAPK in CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes were significantly higher in SLE patients than controls (all p<0.05).
  • CONCLUSION: The inflammation-mediated activation of JNK and p38 MAPK signaling pathways in T and B lymphocytes can be the underlying intracellular mechanisms causing lymphocyte hyperactivity in SLE.



21. Zhu J, Reith ME: Role of the dopamine transporter in the action of psychostimulants, nicotine, and other drugs of abuse. CNS Neurol Disord Drug Targets; 2008 Nov;7(5):393-409
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  • The DA transporter (DAT) is a major target for drugs of abuse in the category of psychostimulants, and for methylphenidate (MPH), a drug used for treating attention deficit hyperactivity disorder (ADHD), which can also be a psychostimulant drug of abuse.
  • In addition, DAT expression is regulated through the removal (internalization) and recycling of the protein from the cell surface.
  • Furthermore, recent studies have demonstrated that individual differences in response to novel environments and psychostimulants can be predicted based on individual basal functional DAT expression.

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  • (PMID = 19128199.001).
  • [ISSN] 1996-3181
  • [Journal-full-title] CNS & neurological disorders drug targets
  • [ISO-abbreviation] CNS Neurol Disord Drug Targets
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA012964; United States / NIDA NIH HHS / DA / DA013261-08; United States / NIDA NIH HHS / DA / DA13261; United States / NIDA NIH HHS / DA / R01 DA013261; United States / NIDA NIH HHS / DA / P50 DA005312; United States / NIDA NIH HHS / DA / R01 DA019676; United States / NIDA NIH HHS / DA / DA19676; United States / NIDA NIH HHS / DA / R01 DA013261-08; United States / NIDA NIH HHS / DA / R21 DA018372; United States / NIDA NIH HHS / DA / R21 DA018372-02; United States / NIDA NIH HHS / DA / R01 DA012964-08; United States / NIDA NIH HHS / DA / DA018372-02; United States / NIDA NIH HHS / DA / R01 DA019676-04; United States / NIDA NIH HHS / DA / P50 DA005312-18; United States / NIDA NIH HHS / DA / DA05312; United States / NIDA NIH HHS / DA / DA018372; United States / NIDA NIH HHS / DA / DA12964
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 0 / Dopamine Plasma Membrane Transport Proteins; 6M3C89ZY6R / Nicotine; VTD58H1Z2X / Dopamine
  • [Number-of-references] 296
  • [Other-IDs] NLM/ NIHMS306957; NLM/ PMC3133725
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22. Apicelli AJ, Maggi LB Jr, Hirbe AC, Miceli AP, Olanich ME, Schulte-Winkeler CL, Saporita AJ, Kuchenreuther M, Sanchez J, Weilbaecher K, Weber JD: A non-tumor suppressor role for basal p19ARF in maintaining nucleolar structure and function. Mol Cell Biol; 2008 Feb;28(3):1068-80
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  • [Title] A non-tumor suppressor role for basal p19ARF in maintaining nucleolar structure and function.
  • However, basal NPM and ARF proteins form nucleolar complexes whose functions remain unknown.
  • Nucleoli from Arf(-/)(-) cells displayed increased nucleolar area, suggesting that basal ARF might regulate key nucleolar functions.
  • Concordantly, ribosome biogenesis and protein synthesis were dramatically elevated in the absence of Arf, causing these cells to exhibit tremendous gains in protein amounts and increases in cell volume.
  • Postmitotic osteoclasts from Arf-null mice exhibited hyperactivity in vitro and in vivo, demonstrating a physiological function for basal ARF.
  • Thus, basal ARF proteins act as a monitor of steady-state ribosome biogenesis and growth independent of their ability to prevent unwarranted hyperproliferation.
  • [MeSH-major] Cell Nucleolus / ultrastructure. Cyclin-Dependent Kinase Inhibitor p16 / physiology. Nuclear Proteins / physiology

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  • (PMID = 18070929.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM066032; United States / NIGMS NIH HHS / GM / GM066032
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Ribosomal; 0 / Nuclear Proteins; 0 / RNA, Ribosomal; 0 / Tumor Suppressor Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC2223401
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23. Traissard N, Herbeaux K, Cosquer B, Jeltsch H, Ferry B, Galani R, Pernon A, Majchrzak M, Cassel JC: Combined damage to entorhinal cortex and cholinergic basal forebrain neurons, two early neurodegenerative features accompanying Alzheimer's disease: effects on locomotor activity and memory functions in rats. Neuropsychopharmacology; 2007 Apr;32(4):851-71
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  • [Title] Combined damage to entorhinal cortex and cholinergic basal forebrain neurons, two early neurodegenerative features accompanying Alzheimer's disease: effects on locomotor activity and memory functions in rats.
  • In Alzheimer's disease (AD), cognitive decline is linked to cholinergic dysfunctions in the basal forebrain (BF), although the earliest neuronal damage is described in the entorhinal cortex (EC).
  • Only rats with combined lesions showed diurnal and nocturnal hyperactivity.
  • [MeSH-minor] Analysis of Variance. Animals. Antibodies, Monoclonal. Behavior, Animal. Cell Count / methods. Choline O-Acetyltransferase / metabolism. Male. Maze Learning / physiology. N-Glycosyl Hydrolases. N-Methylaspartate. Psychomotor Performance / drug effects. Rats. Rats, Long-Evans. Ribosome Inactivating Proteins, Type 1

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  • (PMID = 16760925.001).
  • [ISSN] 0893-133X
  • [Journal-full-title] Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
  • [ISO-abbreviation] Neuropsychopharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 192 IgG-saporin; 0 / Antibodies, Monoclonal; 0 / Ribosome Inactivating Proteins, Type 1; 6384-92-5 / N-Methylaspartate; EC 2.3.1.6 / Choline O-Acetyltransferase; EC 3.2.2.- / N-Glycosyl Hydrolases; N9YNS0M02X / Acetylcholine
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24. Blandini F, Levandis G, Bazzini E, Nappi G, Armentero MT: Time-course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations following intrastriatal injection of 6-hydroxydopamine in the rat: new clues from an old model. Eur J Neurosci; 2007 Jan;25(2):397-405
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  • [Title] Time-course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations following intrastriatal injection of 6-hydroxydopamine in the rat: new clues from an old model.
  • To gain new information from such a classic model, we studied the time-course of the nigrostriatal damage, metabolic changes in the basal ganglia nuclei (cytochrome oxidase activity) and behavioural modifications (rotational response to apomorphine) following unilateral injection of 6-OHDA into the corpus striatum of rat, over a 4-week period.
  • Striatal infusion of 6-OHDA caused early damage of dopaminergic terminals, followed by a slowly evolving loss of dopaminergic cell bodies in the substantia nigra pars compacta, which became apparent during the second week post-injection and peaked at the 28th day post-infusion; the rotational response to apomorphine was already present at the first time point considered (Day 1), and remained substantially stable throughout the 4-week period of observation.
  • The evolution of the nigrostriatal lesion was accompanied by complex changes in the metabolic activity of the other basal ganglia nuclei investigated (substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and subthalamic nucleus), which led, ultimately, to a generalized, metabolic hyperactivity, ipsilaterally to the lesion.
  • However, peculiar patterns of metabolic activation, or inhibition, characterized the post-lesional responses of each nucleus, in the early and intermediate phases, with peculiar response profiles that varied closely related to the functional position occupied within the basal ganglia circuitry.
  • [MeSH-major] Basal Ganglia. Behavior, Animal / drug effects. Oxidopamine. Parkinson Disease, Secondary. Substantia Nigra / pathology
  • [MeSH-minor] Animals. Cell Death / drug effects. Cytochromes c / metabolism. Disease Models, Animal. Immunohistochemistry / methods. Male. Rats. Rats, Sprague-Dawley. Time Factors. Tyrosine 3-Monooxygenase / metabolism

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  • (PMID = 17284180.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 8HW4YBZ748 / Oxidopamine; 9007-43-6 / Cytochromes c; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
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25. Tunc E, Erdogan D, Gozil R, Bahcelioglu M, Calguner E, Take G, Caglar G, Oktem H: Dose-dependent immunohistochemical changes in rat cornea and retina after oral methylphenidate administration. Anat Histol Embryol; 2009 Apr;38(2):128-32
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  • Methylphenidate hydrochloride (MPH), more commonly known as Ritalin, is a piperidine derivative and is the drug most often used to treat attention deficit/hyperactivity disorder, one of the most common behavioural disorders of children and young adults.
  • In our study, we observed that the cornea D2 receptor reactivity showed a dose-related increase after MPH treatment, especially in basal cells of the epithelium and a dose-dependent decrease in the retinal ganglion cell which was statistically meaningful.
  • Apoptotic cell number showed a meaningful increase in the high dose treated group compared to the other groups of the study.

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  • (PMID = 19007354.001).
  • [ISSN] 1439-0264
  • [Journal-full-title] Anatomia, histologia, embryologia
  • [ISO-abbreviation] Anat Histol Embryol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 0 / Receptors, Dopamine; 207ZZ9QZ49 / Methylphenidate
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26. Palomero-Gallagher N, Schleicher A, Lindemann S, Lessenich A, Zilles K, Löscher W: Receptor fingerprinting the circling ci2 rat mutant: insights into brain asymmetry and motor control. Exp Neurol; 2008 Apr;210(2):624-37
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  • Since it is more likely that imbalances in several neurotransmitter systems result in the cascade of neurochemical disturbances underlying disorders involving motor dysfunctions, we measured the densities of 12 neurotransmitter receptors in the basal ganglia and vestibular nuclei of adult circling mutants (ci2/ci2), non-circling littermates (ci2/+) and controls from the background strain (LEW/Ztm).
  • Hyperactivity level of mutants was positively correlated with the adenosine A2A receptor densities in the ipsilateral Acb, but negatively correlated with those of the ipsilateral thalamus.
  • [MeSH-major] Behavior, Animal / physiology. Brain / pathology. Hyperkinesis. Peptide Mapping / methods. Rats, Mutant Strains / abnormalities. Receptors, Cell Surface / metabolism

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  • (PMID = 18255063.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Cell Surface
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27. Moreno G, Perelló M, Camihort G, Luna G, Console G, Gaillard RC, Spinedi E: Impact of transient correction of increased adrenocortical activity in hypothalamo-damaged, hyperadipose female rats. Int J Obes (Lond); 2006 Jan;30(1):73-82
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  • Circulating levels of several hormones, in basal and after i.v. high-glucose load conditions, and RP adiposity morphology and function were then evaluated.
  • These characteristics were fully reversed after transient correction of corticoadrenal hyperactivity induced by AE.

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  • (PMID = 16231033.001).
  • [ISSN] 0307-0565
  • [Journal-full-title] International journal of obesity (2005)
  • [ISO-abbreviation] Int J Obes (Lond)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Glucocorticoids; 0 / Insulin; 0 / Leptin; 7S5I7G3JQL / Dexamethasone; W81N5U6R6U / Sodium Glutamate; W980KJ009P / Corticosterone
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28. Rondou P, Haegeman G, Vanhoenacker P, Van Craenenbroeck K: BTB Protein KLHL12 targets the dopamine D4 receptor for ubiquitination by a Cul3-based E3 ligase. J Biol Chem; 2008 Apr 25;283(17):11083-96
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  • The D4 receptor has a remarkable polymorphism in its third intracellular loop, which is under intensive investigation and which has been associated with, among other conditions, attention deficit hyperactivity disorder.
  • In addition, we show that also other dopamine receptor subtypes undergo basal ubiquitination, but this is not affected by KLHL12.

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  • (PMID = 18303015.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CUL3 protein, human; 0 / Cullin Proteins; 0 / KLHL12 protein, human; 0 / KLHL12 protein, mouse; 0 / Microfilament Proteins; 0 / Receptors, Dopamine; 137750-34-6 / Receptors, Dopamine D4; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2431063
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29. Nakahara S, Tamura M, Matsuki N, Koyama R: Neuronal hyperactivity sustains the basal dendrites of immature dentate granule cells: time-lapse confocal analysis using hippocampal slice cultures. Hippocampus; 2009 Apr;19(4):379-91
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  • [Title] Neuronal hyperactivity sustains the basal dendrites of immature dentate granule cells: time-lapse confocal analysis using hippocampal slice cultures.
  • In the epileptic hippocampus, mature dentate granule cells (GCs) possess basal dendrites (BDs), which is abnormal and is assumed to contribute to seizure progression.
  • However, there is a lack of direct time-lapse evidence showing that neuronal hyperactivity regulates the dendritic development of GCs.
  • These effects were blocked by coapplying tetrodotoxin, a sodium channel blocker, thus convincing us that neuronal hyperactivity contributes to the maintenance of BDs.
  • These results, for the first time, provide us with direct evidence that neuronal hyperactivity contributes to the stability of pre-existing BDs.
  • [MeSH-minor] Action Potentials. Analysis of Variance. Animals. Calbindins. Cell Shape. Electroporation. Green Fluorescent Proteins. Immunohistochemistry. In Vitro Techniques. Microscopy, Confocal. Picrotoxin. Pseudopodia / ultrastructure. Rats. Rats, Sprague-Dawley. S100 Calcium Binding Protein G / metabolism. Sodium Channel Blockers / pharmacology. Tetrodotoxin / pharmacology

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  • (PMID = 19004014.001).
  • [ISSN] 1098-1063
  • [Journal-full-title] Hippocampus
  • [ISO-abbreviation] Hippocampus
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calbindins; 0 / S100 Calcium Binding Protein G; 0 / Sodium Channel Blockers; 124-87-8 / Picrotoxin; 147336-22-9 / Green Fluorescent Proteins; 4368-28-9 / Tetrodotoxin
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30. Karlsson RM, Hefner KR, Sibley DR, Holmes A: Comparison of dopamine D1 and D5 receptor knockout mice for cocaine locomotor sensitization. Psychopharmacology (Berl); 2008 Sep;200(1):117-27
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  • RESULTS: D1R KO showed modest basal hyperactivity and increased center exploration relative to WT.

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  • (PMID = 18600316.001).
  • [ISSN] 0033-3158
  • [Journal-full-title] Psychopharmacology
  • [ISO-abbreviation] Psychopharmacology (Berl.)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AA000411-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Receptors, Dopamine D1; 137750-35-7 / Receptors, Dopamine D5; I5Y540LHVR / Cocaine
  • [Other-IDs] NLM/ NIHMS56410; NLM/ PMC2586326
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31. Richards AB, Scheel TA, Wang K, Henkemeyer M, Kromer LF: EphB1 null mice exhibit neuronal loss in substantia nigra pars reticulata and spontaneous locomotor hyperactivity. Eur J Neurosci; 2007 May;25(9):2619-28
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  • [Title] EphB1 null mice exhibit neuronal loss in substantia nigra pars reticulata and spontaneous locomotor hyperactivity.
  • The molecular mechanisms that regulate basal ganglia development are largely unknown.
  • Eph receptor tyrosine kinases are potential participants in this process as they regulate development of other CNS regions and are expressed in basal ganglia nuclei, such as the substantia nigra (SN) and striatum.
  • Behavioral evaluation of EphB1 null mice in an open-field environment revealed that these mice exhibited spontaneous locomotor hyperactivity.

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  • (PMID = 17561836.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH066332; United States / NINDS NIH HHS / NS / NS27054; United States / NINDS NIH HHS / NS / NS38266; United States / NINDS NIH HHS / NS / NS66332
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers; 3KX376GY7L / Glutamic Acid; 56-12-2 / gamma-Aminobutyric Acid; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; EC 2.7.10.1 / Receptor, EphB1; EC 3.2.1.23 / beta-Galactosidase; VTD58H1Z2X / Dopamine
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32. Marzo N, Ortega S, Stratmann T, García A, Ríos M, Giménez A, Gomis R, Mora C: Cyclin-dependent kinase 4 hyperactivity promotes autoreactivity in the immune system but protects pancreatic cell mass from autoimmune destruction in the nonobese diabetic mouse model. J Immunol; 2008 Jan 15;180(2):1189-98
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  • [Title] Cyclin-dependent kinase 4 hyperactivity promotes autoreactivity in the immune system but protects pancreatic cell mass from autoimmune destruction in the nonobese diabetic mouse model.
  • Cyclin-dependent kinase 4 (Cdk4) plays a central role in perinatal pancreatic beta cell replication, thus becoming a potential target for therapeutics in autoimmune diabetes.
  • Its hyperactive form, Cdk4R24C, causes beta cell hyperplasia without promoting hypoglycemia in a nonautoimmune-prone mouse strain.
  • In this study, we explore whether beta cell hyperproliferation induced by the Cdk4R24C mutation balances the autoimmune attack against beta cells inherent to the NOD genetic background.
  • In this study, we show that NOD/Cdk4R24C knockin mice exhibit exacerbated diabetes and insulitis, and that this exacerbated diabetic phenotype is solely due to the hyperactivity of the NOD/Cdk4R24C immune repertoire.
  • Accordingly, NOD/Cdk4R24C splenocytes show increased basal proliferation and higher activation markers expression compared with NOD/WT splenocytes.
  • NOD/SCID/Cdk4R24C knockin mice develop beta cell hyperplasia spontaneously.
  • Thus, the Cdk4R24C mutation opens two avenues in the NOD model: when expressed specifically in beta cells, it provides a new potential strategy for beta cell regeneration in autoimmune diabetes, but its expression in the immune repertoire exacerbates autoimmunity.

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  • (PMID = 18178859.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.22 / Cdk4 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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33. Babovic D, Jiang L, Gantois I, Lawrence AJ, Ferreri V, Schütz G, Waddington JL, Drago J: Age-related behavioural phenotype and cellular characterisation of mice with progressive ablation of D1 dopamine receptor-expressing cells. Behav Brain Res; 2010 Jan 5;206(1):78-87
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  • While MUT mice evidenced hyperactivity over initial exploration at both time points, the topography of hyperactivity shifted.
  • Moreover, initial hyperactivity was sustained over habituation at 12 weeks, but not at 22 weeks.
  • Quantitative autoradiography at 20 weeks revealed loss of D1-like dopamine receptor binding in the entire basal ganglia, with upregulated D2-like binding.
  • Understanding the mechanistic bases of mitigation vs persistence of individual phenotypes in relation to neural adaptation consequent to cell loss may lead to novel therapeutic strategies for basal ganglia disorders.

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  • (PMID = 19733597.001).
  • [ISSN] 1872-7549
  • [Journal-full-title] Behavioural brain research
  • [ISO-abbreviation] Behav. Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Dopamine D1; 0 / Receptors, Dopamine D2
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34. Schirmer M, Kaiser A, Lessenich A, Lindemann S, Fedrowitz M, Gernert M, Löscher W: Auditory and vestibular defects and behavioral alterations after neonatal administration of streptomycin to Lewis rats: Similarities and differences to the circling (ci2/ci2) Lewis rat mutant. Brain Res; 2007 Jun 25;1155:179-95
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  • In rodents, damage to the inner ear is often associated with rotational behavior and locomotor hyperactivity reminiscent of such behaviors resulting from an imbalance of forebrain dopamine systems.
  • Based on previous observations in the circling (ci2/ci2) Lewis (LEW) rat mutant, a spontaneous mutation leading to hair cell loss, deafness, impairment of vestibular functions, lateralized circling, hyperactivity and alterations in the nigrostriatal dopamine system, we have recently hypothesized that vestibular defects during postnatal development, independent of whether induced or inherited, lead to secondary changes in the dopaminergic system within the basal ganglia, which would be a likely explanation for the typical behavioral phenotype seen in such models.

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  • (PMID = 17493596.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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35. Sukhodolsky DG, Leckman JF, Rothenberger A, Scahill L: The role of abnormal neural oscillations in the pathophysiology of co-occurring Tourette syndrome and attention-deficit/hyperactivity disorder. Eur Child Adolesc Psychiatry; 2007 Jun;16 Suppl 1:51-9
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  • [Title] The role of abnormal neural oscillations in the pathophysiology of co-occurring Tourette syndrome and attention-deficit/hyperactivity disorder.
  • OBJECTIVE: To examine the role of aberrant neural oscillatory activity in the pathophysiology of co-occurring Tourette Syndrome (TS) and Attention-Deficit/Hyperactivity Disorder (ADHD).
  • RESULTS: Structural and functional abnormalities in the cortical-striatal-thalamo-cortical circuits may result in the disruption of oscillatory activity within the basal ganglia of individuals with TS and lead to transient hyperpolarization of selected thalamocortical regions.
  • [MeSH-major] Attention Deficit Disorder with Hyperactivity / physiopathology. Brain / physiopathology. Tourette Syndrome / physiopathology

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  • [ErratumIn] Eur Child Adolesc Psychiatry. 2007 Dec;16(8):537
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  • (PMID = 17665283.001).
  • [ISSN] 1018-8827
  • [Journal-full-title] European child & adolescent psychiatry
  • [ISO-abbreviation] Eur Child Adolesc Psychiatry
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 131
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36. Demura M, Bulun SE: CpG dinucleotide methylation of the CYP19 I.3/II promoter modulates cAMP-stimulated aromatase activity. Mol Cell Endocrinol; 2008 Feb 13;283(1-2):127-32
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  • Aromatase promoter I.3/II, regulated by a cAMP response element (CRE), is normally quiescent in human skin fibroblasts, whereas its hyperactivity may cause local or systemic estrogen excess.
  • Basal and cAMP-stimulated aromatase activity and promoter I.3/II activation were significantly higher in the presence of unmethylated DNA.

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  • (PMID = 18201819.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / C67167
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / RNA, Messenger; E0399OZS9N / Cyclic AMP; EC 1.14.14.1 / Aromatase
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37. Fukabori R, Kobayashi K: [Functional analysis of the roles of direct and indirect pathways by using immunotoxin-mediated cell targeting approach]. Brain Nerve; 2009 Apr;61(4):412-8
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  • [Title] [Functional analysis of the roles of direct and indirect pathways by using immunotoxin-mediated cell targeting approach].
  • The neural circuit connecting the cerebral cortex and the basal ganglia mediates a variety of brain functions including voluntary movement, motor learning, and reinforcement learning.
  • The pathogenesis of certain neurological and neuropsychiatric diseases involves the dysfunction of these dopamin systems; some of these diseases include Parkinson's disease, schizophrenia, and attention deficit hyperactivity disorder.
  • Immunotoxin-mediated cell targeting is an approach employed in transgenic animals to eliminated specific neuronal types from a neuronal circuitry.
  • Here, we describe the use of immunotoxin-mediated cell targeting for studying the neural circuitry that underlies the motor behavior demonstrated in response to systemic dopamine stimulation; further, we propose the potential mechanism that controls direct and indirect striatal pathway-dependent behavior.
  • [MeSH-major] Basal Ganglia / physiology. Cerebral Cortex / physiology. Immunotoxins. Neural Pathways / physiology. Neurons / physiology

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  • (PMID = 19378811.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunotoxins; VTD58H1Z2X / Dopamine
  • [Number-of-references] 38
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38. Matthies HJ, Moore JL, Saunders C, Matthies DS, Lapierre LA, Goldenring JR, Blakely RD, Galli A: Rab11 supports amphetamine-stimulated norepinephrine transporter trafficking. J Neurosci; 2010 Jun 9;30(23):7863-77
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  • NET is also a major target for medications used for the treatment of depression, attention deficit/hyperactivity disorder, narcolepsy, and obesity.
  • In this study, we used a recently developed NET antibody and the presence of large presynaptic boutons in sympathetic neurons to examine basal and AMPH-modulated NET trafficking.

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  • (PMID = 20534835.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA013975-04; United States / NIDA NIH HHS / DA / DA13975; United States / NIDA NIH HHS / DA / R01 DA013975; United States / NIDA NIH HHS / DA / DA013975-04; United States / NIMH NIH HHS / MH / MH05892; United States / NIDA NIH HHS / DA / R56 DA013975
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic Agents; 0 / Carrier Proteins; 0 / Membrane Proteins; 0 / Norepinephrine Plasma Membrane Transport Proteins; 0 / Rab11-FIP2 protein, rat; CK833KGX7E / Amphetamine; EC 3.6.1.- / rab GTP-Binding Proteins; EC 3.6.1.- / rab11 protein; EC 3.6.5.2 / rab4 GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS212070; NLM/ PMC2935280
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39. Huleihel R, Yanai J: Disruption of the development of cholinergic-induced translocation/activation of PKC isoforms after prenatal heroin exposure. Brain Res Bull; 2006 Mar 31;69(2):174-81
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  • Prenatal exposure of mice to heroin resulted in behavioral deficits present at adulthood, and related to septohippocampal cholinergic innervation accompanied by both pre- and postsynaptic cholinergic hyperactivity; including an increase in membrane PKC activity, and a desensitization of PKC to cholinergic input, which correlated highly with the behavioral performance, and was reversed by cholinergic grafting.
  • Prenatal heroin exposure increased basal PKCgamma, beta and alpha levels.

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  • (PMID = 16533667.001).
  • [ISSN] 0361-9230
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / HD 40820
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 0 / Cholinergic Agonists; 0 / Protein Isoforms; 0 / Receptors, Cholinergic; 70D95007SX / Heroin; EC 2.7.11.13 / Protein Kinase C; N9YNS0M02X / Acetylcholine
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40. Soulage C, Zarrouki B, Soares AF, Lagarde M, Geloen A: Lou/C obesity-resistant rat exhibits hyperactivity, hypermetabolism, alterations in white adipose tissue cellularity, and lipid tissue profiles. Endocrinology; 2008 Feb;149(2):615-25
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  • [Title] Lou/C obesity-resistant rat exhibits hyperactivity, hypermetabolism, alterations in white adipose tissue cellularity, and lipid tissue profiles.
  • Basal lipolysis and sensitivity to noradrenaline were similar; however, the responsiveness to noradrenaline was lower in adipocytes from Lou/C compared with that from Wistar rats.
  • [MeSH-minor] Animals. Cell Count. Fatty Acid Synthase, Type I / genetics. Fatty Acids / metabolism. Lipolysis / physiology. Lipoprotein Lipase / genetics. Male. Motor Activity / physiology. Norepinephrine / pharmacology. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Species Specificity. Stearoyl-CoA Desaturase / genetics. Stearoyl-CoA Desaturase / metabolism. Sympathetic Nervous System / physiology. Sympathomimetics / pharmacology

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  • (PMID = 18006635.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Sympathomimetics; EC 1.14.19.1 / Scd1 protein, mouse; EC 1.14.19.1 / Stearoyl-CoA Desaturase; EC 2.3.1.85 / Fatty Acid Synthase, Type I; EC 3.1.1.34 / Lipoprotein Lipase; X4W3ENH1CV / Norepinephrine
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41. Drgon T, Lin Z, Wang GJ, Fowler J, Pablo J, Mash DC, Volkow N, Uhl GR: Common human 5' dopamine transporter (SLC6A3) haplotypes yield varying expression levels in vivo. Cell Mol Neurobiol; 2006 Jul-Aug;26(4-6):875-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] 5' Flanking Region. Adult. Attention Deficit Disorder with Hyperactivity / metabolism. Basal Ganglia / metabolism. Base Sequence. Female. Gene Expression. Gene Frequency. Humans. Male. Molecular Sequence Data. Sequence Analysis, DNA. Sequence Homology, Nucleic Acid

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  • (PMID = 16710758.001).
  • [ISSN] 0272-4340
  • [Journal-full-title] Cellular and molecular neurobiology
  • [ISO-abbreviation] Cell. Mol. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA 06227; United States / NIDA NIH HHS / DA / DA 7092-01; United States / NIDA NIH HHS / DA / DA00280; United States / NIDA NIH HHS / DA / DA09490-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Plasma Membrane Transport Proteins; 0 / SLC6A3 protein, human
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42. Beaulieu JM, Sotnikova TD, Gainetdinov RR, Caron MG: Paradoxical striatal cellular signaling responses to psychostimulants in hyperactive mice. J Biol Chem; 2006 Oct 27;281(43):32072-80
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  • Here we used dopamine transporter knock-out mice to examine which particular changes in the regulation of these cell signaling mechanisms are associated with distinct behavioral responses to psychostimulants.
  • However, in dopamine transporter knock-out mice that display a hyperactivity phenotype resulting from a persistent hyperdopaminergic state, these drugs antagonize hyperactivity.
  • Under basal conditions, dopamine transporter knock-out mice show enhanced striatal DARPP-32 phosphorylation, activation of ERK, and inactivation of Akt as compared with wild-type littermates.
  • However, administration of amphetamine or methylphenidate to these mice reveals that inhibition of ERK signaling is a common determinant for the ability of these drugs to antagonize hyperactivity.
  • In contrast, psychostimulants activate ERK and induce hyperactivity in normal animals.
  • These data suggest that the inhibitory action of psychostimulants on dopamine-dependent hyperactivity results from altered regulation of striatal ERK signaling.
  • In addition, these results illustrate how altered homeostatic state of neurotransmission can influence in vivo signaling responses and biological actions of pharmacological agents used to manage psychiatric conditions such as Attention Deficit Hyperactivity Disorder (ADHD).

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  • (PMID = 16954211.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA 13511; United States / NIMH NIH HHS / MH / MH 40159; United States / NIMH NIH HHS / MH / MH 73853; United States / NINDS NIH HHS / NS / NS 19576
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 0 / Phosphoproteins; 0 / Psychotropic Drugs; 0 / Serotonin Receptor Agonists; 207ZZ9QZ49 / Methylphenidate; 333DO1RDJY / Serotonin; 74885-09-9 / 5-carboxamidotryptamine; CK833KGX7E / Amphetamine
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43. Kintaka Y, Osaka T, Suzuki Y, Hashiguchi T, Niijima A, Kageyama H, Fumiko T, Shioda S, Inoue S: Effects of gastric vagotomy on visceral cell proliferation induced by ventromedial hypothalamic lesions: role of vagal hyperactivity. J Mol Neurosci; 2009 Jul;38(3):243-9
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  • [Title] Effects of gastric vagotomy on visceral cell proliferation induced by ventromedial hypothalamic lesions: role of vagal hyperactivity.
  • In rats, ventromedial hypothalamic (VMH) lesions induce cell proliferation in the visceral organs (stomach, small intestine, liver, and pancreas) due to hyperactivity of the vagus nerve.
  • To investigate the effects of selective gastric vagotomy on VMH lesion-induced cell proliferation and secretion of gastric acid, we assessed the mitotic index (the number of proliferating cell nuclear antigen (PCNA)-immunopositive cells per 1,000 cells in the gastric mucosal cell layer) and measured the volume of secreted basal gastric acid.
  • VMH lesions resulted in an increased mitotic index and thickness of the gastric mucosal cell layer and gave rise to the hypersecretion of gastric acid.
  • Selective gastric vagotomy restored these parameters to normal without affecting cell proliferation in other visceral organs.
  • These results suggest that VMH lesion-induced vagally mediated cell proliferation in the visceral organs is associated with hyperfunction in these organs, and VMH lesion-induced resistance to ethanol may be due to thickening of the gastric mucosal cell layer resulting from cell proliferation in the gastric mucosa-this in turn is due to hyperactivity of the vagus nerve.
  • [MeSH-major] Cell Proliferation. Gastric Mucosa. Vagotomy. Vagus Nerve / physiology. Ventromedial Hypothalamic Nucleus / pathology

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  • (PMID = 19455436.001).
  • [ISSN] 0895-8696
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Müller Smith K, Fagel DM, Stevens HE, Rabenstein RL, Maragnoli ME, Ohkubo Y, Picciotto MR, Schwartz ML, Vaccarino FM: Deficiency in inhibitory cortical interneurons associates with hyperactivity in fibroblast growth factor receptor 1 mutant mice. Biol Psychiatry; 2008 May 15;63(10):953-62
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  • [Title] Deficiency in inhibitory cortical interneurons associates with hyperactivity in fibroblast growth factor receptor 1 mutant mice.
  • BACKGROUND: Motor hyperactivity due to hyper-dopaminergic neurotransmission in the basal ganglia is well characterized; much less is known about the role of the neocortex in controlling motor behavior.
  • RESULTS: Fgfr1(f/f;hGfapCre) mice have spontaneous locomotor hyperactivity characterized by longer bouts of locomotion and fewer resting points that is significantly reduced by the D1 and D2 receptor antagonists.
  • The decrease in parvalbumin+ interneurons in cortex correlated with the extent of hyperactivity.

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  • (PMID = 17988653.001).
  • [ISSN] 1873-2402
  • [Journal-full-title] Biological psychiatry
  • [ISO-abbreviation] Biol. Psychiatry
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH067715; United States / NIMH NIH HHS / MH / T32 MH018268; United States / NIMH NIH HHS / MH / 5R01MH067715-03; United States / NIMH NIH HHS / MH / T32MH18268
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biogenic Monoamines; 0 / Central Nervous System Stimulants; 0 / Dopamine Agents; 0 / Nerve Tissue Proteins; 104781-85-3 / Fibroblast Growth Factor 1; 207ZZ9QZ49 / Methylphenidate; CK833KGX7E / Amphetamine; EC 4.1.1.15 / Glutamate Decarboxylase; EC 4.1.1.15 / glutamate decarboxylase 1
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45. Barlow PW, Kurczyńska EU: The anatomy of the chi-chi of Ginkgo biloba suggests a mode of elongation growth that is an alternative to growth driven by an apical meristem. J Plant Res; 2007 Mar;120(2):269-80
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  • Towards the base of the chi-chi, the fusiform cells and young tracheids were aligned parallel to the axis, indicating that the orientation of the cambial cells in basal regions of the chi-chi gradually became normalised as the tip of the chi-chi extended forwards.
  • Nevertheless, in such basal sites, tracheids near the centre of the chi-chi showed variable orientations in accordance with their mode of formation during the early stages of chi-chi development.
  • The initiation of a chi-chi is proposed to derive from a localised hyperactivity of vascular cambial-cell production in the supporting stem.

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  • [ISSN] 0918-9440
  • [Journal-full-title] Journal of plant research
  • [ISO-abbreviation] J. Plant Res.
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  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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46. Sakatani S, Yamada K, Homma C, Munesue S, Yamamoto Y, Yamamoto H, Hirase H: Deletion of RAGE causes hyperactivity and increased sensitivity to auditory stimuli in mice. PLoS One; 2009;4(12):e8309
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  • [Title] Deletion of RAGE causes hyperactivity and increased sensitivity to auditory stimuli in mice.
  • The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor that belongs to the immunoglobulin superfamily of cell surface receptors.
  • However, how RAGE influences gross behavioral activity patterns in basal condition has not been addressed to date.

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  • (PMID = 20016851.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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47. Wang XL, Zhang HM, Chen SR, Pan HL: Altered synaptic input and GABAB receptor function in spinal superficial dorsal horn neurons in rats with diabetic neuropathy. J Physiol; 2007 Mar 15;579(Pt 3):849-61
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  • Hyperactivity of spinal dorsal horn neurons plays an important role in the development of diabetic neuropathic pain.
  • To determine the changes in synaptic input to dorsal horn neurons and the GABAB)receptor function in streptozotocin-induced diabetes, we performed whole-cell recording (GDP-beta-S included in the internal solution) on lamina II neurons in rat spinal cord slices.
  • On the other hand, the basal frequency and amplitude of GABAergic spontaneous IPSCs and mIPSCs and those of glycinergic spontaneous IPSCs and mIPSCs did not differ significantly between control and diabetic rats.

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  • (PMID = 17218355.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM064830; United States / NINDS NIH HHS / NS / R01 NS045602; United States / NIGMS NIH HHS / GM / GM64830; United States / NINDS NIH HHS / NS / NS45602
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GABA Agonists; 0 / GABA Antagonists; 0 / Receptors, GABA-B; 3KX376GY7L / Glutamic Acid; H789N3FKE8 / Baclofen; TE7660XO1C / Glycine; Y37615DVKC / Bicuculline
  • [Other-IDs] NLM/ PMC2151355
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48. Aydin C, Aytan N, Mahon MJ, Tawfeek HA, Kowall NW, Dedeoglu A, Bastepe M: Extralarge XL(alpha)s (XXL(alpha)s), a variant of stimulatory G protein alpha-subunit (Gs(alpha)), is a distinct, membrane-anchored GNAS product that can mimic Gs(alpha). Endocrinology; 2009 Aug;150(8):3567-75
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  • XXL(alpha)s-R844H, which bears a mutation analogous to that in the constitutively active Gs(alpha) mutant Gs(alpha)-R201H (gsp oncogene), displayed elevated basal signaling.
  • Our findings suggest that XXL(alpha)s deficiency or hyperactivity may contribute to the pathogenesis of diseases caused by GNAS mutations.

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  • (PMID = 19423757.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK073911; United States / NIA NIH HHS / AG / P30 AG013846; United States / NIDDK NIH HHS / DK / DK073911-01A2; United States / NIDDK NIH HHS / DK / R01 DK073911-01A2; United States / NIA NIH HHS / AG / P30AG13846; United States / NIDDK NIH HHS / DK / R01DK073911
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / DNA, Complementary; 0 / RNA, Messenger; E0399OZS9N / Cyclic AMP; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Other-IDs] NLM/ PMC2717877
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49. Adriani W, Canese R, Podo F, Laviola G: 1H MRS-detectable metabolic brain changes and reduced impulsive behavior in adult rats exposed to methylphenidate during adolescence. Neurotoxicol Teratol; 2007 Jan-Feb;29(1):116-25
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  • Administration of methylphenidate (MPH, Ritalin) to children affected by attention deficit hyperactivity disorder (ADHD) is an elective therapy, which however raises concerns for public health, due to possible persistent neuro-behavioral alterations.
  • MPH-exposed animals showed a less marked shifting profile from the large/late to the small/soon reward, suggesting reduced basal levels of impulsivity, compared to controls.

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  • (PMID = 17196789.001).
  • [ISSN] 0892-0362
  • [Journal-full-title] Neurotoxicology and teratology
  • [ISO-abbreviation] Neurotoxicol Teratol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 207ZZ9QZ49 / Methylphenidate
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50. Imamov O, Yakimchuk K, Morani A, Schwend T, Wada-Hiraike O, Razumov S, Warner M, Gustafsson JA: Estrogen receptor beta-deficient female mice develop a bladder phenotype resembling human interstitial cystitis. Proc Natl Acad Sci U S A; 2007 Jun 5;104(23):9806-9
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  • We found that, in the bladders of WT mice, ERbeta is expressed in the basal cell layer of the urothelium.
  • The hyperactivity of T cells may be because of an imbalance between ERalpha and ERbeta signaling in female ERbeta(-/-) mice.

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  • (PMID = 17522255.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor beta; 0 / Glycosaminoglycans; 0 / glucosaminoglycans
  • [Other-IDs] NLM/ PMC1887607
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51. Budziszewska B, Lasoń W, Steczkowska M, Gergont A: [Value of the experiment for developmental neurology]. Przegl Lek; 2009;66(11):958-62
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  • The etiology of autism is not known and there is no drug for ameliorating basal symptoms of this disease.
  • Therapeutic action of psychostimulant drugs in the attention deficit hyperactivity disorder (ADHD) are known for years, but because of their addictive properties, decision about their clinical use in a child is not easy.
  • The introduction of efficient neuroprotective drugs, which may ameliorate secondary neuronal cell damage in various brain regions to the therapy is the main aim of numerous experimental works.

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  • (PMID = 20297638.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Neuroprotective Agents
  • [Number-of-references] 37
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52. Hill M, Anney RJ, Gill M, Hawi Z: Functional analysis of intron 8 and 3' UTR variable number of tandem repeats of SLC6A3: differential activity of intron 8 variants. Pharmacogenomics J; 2010 Oct;10(5):442-7
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  • Association studies have found that variation in the dopamine transporter gene (SLC6A3) is important in the susceptibility to attention-deficit hyperactivity disorder (ADHD) and response to methylphenidate treatment.
  • We assessed the relative activity of variable number tandem repeat (VNTR) alleles of SLC6A3 under basal and stimulated cellular conditions, as well as in the presence of pharmacological blockade of the dopamine transporter using gene-reporter constructs.
  • The lack of enhanced allele-specific activity in response to treatment regimes suggests that differential activity under basal conditions is the primary mode of action.
  • [MeSH-minor] Alleles. Attention Deficit Disorder with Hyperactivity / drug therapy. Attention Deficit Disorder with Hyperactivity / genetics. Cell Culture Techniques. Cell Line, Tumor. Colforsin / pharmacology. Dopamine Uptake Inhibitors / therapeutic use. Genes, Reporter. Genetic Vectors. Humans. Luciferases / genetics. Methylphenidate / therapeutic use. Piperazines / pharmacology. Transfection

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  • (PMID = 20029387.001).
  • [ISSN] 1473-1150
  • [Journal-full-title] The pharmacogenomics journal
  • [ISO-abbreviation] Pharmacogenomics J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Dopamine Plasma Membrane Transport Proteins; 0 / Dopamine Uptake Inhibitors; 0 / Piperazines; 0 / SLC6A3 protein, human; 1F7A44V6OU / Colforsin; 207ZZ9QZ49 / Methylphenidate; 76778-22-8 / GBR 12935; EC 1.13.12.- / Luciferases
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53. Joho RH, Street C, Matsushita S, Knöpfel T: Behavioral motor dysfunction in Kv3-type potassium channel-deficient mice. Genes Brain Behav; 2006 Aug;5(6):472-82
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  • The voltage-gated potassium channels Kv3.1 and Kv3.3 are expressed in several distinct neuronal subpopulations in brain areas known to be involved in motor control such as cortex, basal ganglia and cerebellum.
  • Depending on the lack of Kv3.1 or Kv3.3 channel subunits, mutant mice show different Kv3-null allele-dependent behavioral alterations that include constitutive hyperactivity, sleep loss, impaired motor performance and, in the case of the Kv3.1/Kv3.3 double mutant, also severe ataxia, tremor and myoclonus (Espinosa et al. 2001, J Neurosci 21, 6657-6665, Genes, Brain Behav 3, 90-100).
  • The lack of Kv3.1 channel subunits is mainly responsible for the constitutively increased locomotor activity and for sleep loss, whereas the absence of Kv3.3 subunits affects cerebellar function, in particular Purkinje cell discharges and olivocerebellar system properties (McMahon et al. 2004, Eur J Neurosci 19, 3317-3327).



54. Kraus KS, Ding D, Zhou Y, Salvi RJ: Central auditory plasticity after carboplatin-induced unilateral inner ear damage in the chinchilla: up-regulation of GAP-43 in the ventral cochlear nucleus. Hear Res; 2009 Sep;255(1-2):33-43
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  • In this study, we documented the relationship between carboplatin-induced hair cell degeneration and VCN plasticity in the chinchilla.
  • Unilateral application of carboplatin (5mg/ml) on the round window membrane resulted in massive hair cell loss.
  • Outer hair cell degeneration showed a pronounced basal-to-apical gradient while inner hair cell loss was more equally distributed throughout the cochlea.
  • In VCN, the high-frequency area dorsally showed slightly yet significantly stronger GAP-43 up-regulation than the low-frequency area ventrally, possibly reflecting the high-to-low frequency gradient of hair cell degeneration.
  • Alternatively, massive fiber growth may represent a deleterious process causing central hyperactivity that leads to loudness recruitment or tinnitus.

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  • (PMID = 19435600.001).
  • [ISSN] 1878-5891
  • [Journal-full-title] Hearing research
  • [ISO-abbreviation] Hear. Res.
  • [Language] ENG
  • [Grant] United States / NIDCD NIH HHS / DC / R01 DC006630; United States / NIDCD NIH HHS / DC / R01 DC006630-05; United States / NIDCD NIH HHS / DC / R01 DC06630
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / GAP-43 Protein; BG3F62OND5 / Carboplatin
  • [Other-IDs] NLM/ NIHMS139908; NLM/ PMC2777517
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55. Armentero MT, Fancellu R, Nappi G, Bramanti P, Blandini F: Prolonged blockade of NMDA or mGluR5 glutamate receptors reduces nigrostriatal degeneration while inducing selective metabolic changes in the basal ganglia circuitry in a rodent model of Parkinson's disease. Neurobiol Dis; 2006 Apr;22(1):1-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonged blockade of NMDA or mGluR5 glutamate receptors reduces nigrostriatal degeneration while inducing selective metabolic changes in the basal ganglia circuitry in a rodent model of Parkinson's disease.
  • The ionotropic, N-methyl-D-aspartate receptor antagonist MK-801 increased cell survival in the substantia nigra pars compacta (SNc) and corrected the metabolic hyperactivity (increased cytochrome oxidase activity) of the ipsilateral substantia nigra pars reticulata (SNr) associated with the lesion, but showed no effects on the 6-OHDA-induced hyperactivity of the subthalamic nucleus (STN).
  • As opposed to MK-801, MPEP abolished the STN metabolic hyperactivity associated with the nigrostriatal lesion, without affecting SNr activity.
  • Specific modulation of STN hyperactivity obtained with mGluR5 blockade may, therefore, open interesting perspectives for the use of this class of compounds in the treatment of Parkinson's disease.
  • [MeSH-minor] Animals. Cell Survival / drug effects. Cell Survival / physiology. Disease Models, Animal. Dizocilpine Maleate / pharmacology. Dizocilpine Maleate / therapeutic use. Electron Transport Complex IV / drug effects. Electron Transport Complex IV / metabolism. Energy Metabolism / drug effects. Energy Metabolism / physiology. Male. Nerve Degeneration / drug therapy. Nerve Degeneration / physiopathology. Nerve Degeneration / prevention & control. Neuroprotective Agents / pharmacology. Neuroprotective Agents / therapeutic use. Oxidopamine. Pyridines / pharmacology. Pyridines / therapeutic use. Rats. Rats, Sprague-Dawley. Receptor, Metabotropic Glutamate 5. Receptors, Metabotropic Glutamate / antagonists & inhibitors. Receptors, Metabotropic Glutamate / metabolism. Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors. Receptors, N-Methyl-D-Aspartate / metabolism. Subthalamic Nucleus / drug effects. Subthalamic Nucleus / metabolism. Subthalamic Nucleus / physiopathology

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  • (PMID = 16289868.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 6-methyl-2-(phenylethynyl)pyridine; 0 / Excitatory Amino Acid Antagonists; 0 / Grm5 protein, rat; 0 / Neuroprotective Agents; 0 / Pyridines; 0 / Receptor, Metabotropic Glutamate 5; 0 / Receptors, Glutamate; 0 / Receptors, Metabotropic Glutamate; 0 / Receptors, N-Methyl-D-Aspartate; 6LR8C1B66Q / Dizocilpine Maleate; 8HW4YBZ748 / Oxidopamine; EC 1.9.3.1 / Electron Transport Complex IV
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56. Brandt C, Gastens AM, Sun Mz, Hausknecht M, Löscher W: Treatment with valproate after status epilepticus: effect on neuronal damage, epileptogenesis, and behavioral alterations in rats. Neuropharmacology; 2006 Sep;51(4):789-804
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  • A self-sustaining SE was induced by prolonged electrical stimulation of the basal amygdala via a depth electrode.
  • However, treatment with VPA after SE prevented the hyperexcitability and locomotor hyperactivity observed in vehicle-treated epileptic rats.
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Death / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Electric Stimulation / adverse effects. Electroencephalography / methods. Female. Functional Laterality. Hippocampus / drug effects. Hippocampus / pathology. Hyperkinesis / drug therapy. Hyperkinesis / etiology. Maze Learning / drug effects. Motor Activity / drug effects. Rats. Rats, Sprague-Dawley. Rotarod Performance Test / methods. Time Factors

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  • (PMID = 16806297.001).
  • [ISSN] 0028-3908
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 614OI1Z5WI / Valproic Acid
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57. Braunstein KE, Eschbach J, Ròna-Vörös K, Soylu R, Mikrouli E, Larmet Y, René F, Gonzalez De Aguilar JL, Loeffler JP, Müller HP, Bucher S, Kaulisch T, Niessen HG, Tillmanns J, Fischer K, Schwalenstöcker B, Kassubek J, Pichler B, Stiller D, Petersen A, Ludolph AC, Dupuis L: A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons. Hum Mol Genet; 2010 Nov 15;19(22):4385-98
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  • The molecular motor dynein and its associated regulatory subunit dynactin have been implicated in several neurodegenerative conditions of the basal ganglia, such as Huntington's disease (HD) and Perry syndrome, an atypical Parkinson-like disease.
  • However, dynactin is also able to act independently of dynein, and there is currently no direct evidence linking dynein to basal ganglia degeneration.
  • These mice exhibited motor and behavioural abnormalities including hindlimb clasping, early muscle weakness, incoordination and hyperactivity.
  • Our study supports a role for dynein dysfunction in the pathogenesis of neurodegenerative disorders of the basal ganglia, such as Perry syndrome and HD.

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  • (PMID = 20807776.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Microtubule-Associated Proteins; 0 / Receptors, Dopamine D2; 144198-36-7 / dynactin; EC 3.6.4.2 / Dyneins; VTD58H1Z2X / Dopamine
  • [Other-IDs] NLM/ PMC3298848
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58. Yasoshima Y, Kai N, Yoshida S, Shiosaka S, Koyama Y, Kayama Y, Kobayashi K: Subthalamic neurons coordinate basal ganglia function through differential neural pathways. J Neurosci; 2005 Aug 24;25(34):7743-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subthalamic neurons coordinate basal ganglia function through differential neural pathways.
  • The subthalamic nucleus (STN) is a key component of basal ganglia circuitry that mediates a variety of motor functions.
  • The STN neurons send glutamatergic projections to the output structures of basal ganglia, including the substantia nigra pars reticulata (SNr) and the entopeduncular nucleus, and also innervate the globus pallidus (GP).
  • Here we performed conditional ablation of the STN neurons by using immunotoxin-mediated cell targeting.
  • Ablation of the STN neurons increased spontaneous movement and reduced hyperactivity in response to DA stimulation.
  • [MeSH-major] Basal Ganglia / physiology. Neurons / physiology. Subthalamic Nucleus / physiology

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  • (PMID = 16120775.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] VTD58H1Z2X / Dopamine
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