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1
basal cell hyperactivity 2005:2010[pubdate] *count=100
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Items 1 to 62 of about 62
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
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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Hazardous Substances Data Bank.
METHYLPHENIDATE
.
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AMPHETAMINE
.
Hazardous Substances Data Bank.
DIZOCILPINE
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
OMIM: Data: Gene Annotation
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
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Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11062-8
[
11572969.001
]
(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
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
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
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
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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Behav Neurosci. 2008 Jun;122(3):491-7
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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
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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[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
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
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.
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[ISSN]
1540-9538
[Journal-full-title]
The Journal of experimental medicine
[ISO-abbreviation]
J. Exp. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Keratin-14; 0 / Krt1-14 protein, mouse; 0 / Serpins; 0 / Spink5 protein, mouse; EC 3.4.21.- / Kallikreins; EC 3.4.21.- / Klk5 protein, mouse
[Other-IDs]
NLM/ PMC2715042
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
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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Mouse Genome Informatics (MGI)
.
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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
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
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
15.
Le Masurier M, Oldenzeil W, Lehman C, Cowen P, Sharp T:
Effect of acute tyrosine depletion in using a branched chain amino-acid mixture on dopamine neurotransmission in the rat brain.
Neuropsychopharmacology
; 2006 Feb;31(2):310-7
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In microdialysis experiments this amino-acid mixture reduced
basal
and amphetamine-evoked striatal dopamine release, as well as amphetamine-induced
hyperactivity
.
[MeSH-minor]
3,4-Dihydroxyphenylacetic Acid / metabolism. 5-Hydroxytryptophan / metabolism. Amphetamine / pharmacology. Analysis of Variance. Animals. Behavior, Animal / drug effects. Catecholamines / metabolism.
Cell
Count / methods. Dopamine Agents / pharmacology. Dose-Response Relationship, Drug. Drug Interactions. Immunohistochemistry / methods. Male. Microdialysis / methods. Motor Activity / drug effects. Oncogene Proteins v-fos / metabolism. Rats. Rats, Sprague-Dawley. Serotonin / metabolism. Time Factors
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.
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L-TYROSINE
.
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(PMID = 16034439.001).
[ISSN]
0893-133X
[Journal-full-title]
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
[ISO-abbreviation]
Neuropsychopharmacology
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Amino Acids, Branched-Chain; 0 / Catecholamines; 0 / Dopamine Agents; 0 / Oncogene Proteins v-fos; 102-32-9 / 3,4-Dihydroxyphenylacetic Acid; 333DO1RDJY / Serotonin; 42HK56048U / Tyrosine; C1LJO185Q9 / 5-Hydroxytryptophan; CK833KGX7E / Amphetamine; VTD58H1Z2X / Dopamine
16.
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
17.
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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[ISSN]
1542-0086
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Biophysical journal
[ISO-abbreviation]
Biophys. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
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United States
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0 / Antifreeze Proteins; 0 / Ice
[Other-IDs]
NLM/ PMC2426666
18.
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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[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
19.
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
20.
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.
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[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 / Insulin; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
[Other-IDs]
NLM/ PMC2662067
21.
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.
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[ISSN]
1573-2592
[Journal-full-title]
Journal of clinical immunology
[ISO-abbreviation]
J. Clin. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
22.
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
23.
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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Micron. 2000 Apr;31(2):133-41
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[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
24.
Grigorian A, Torossian S, Demetriou M:
T-cell growth, cell surface organization, and the galectin-glycoprotein lattice.
Immunol Rev
; 2009 Jul;230(1):232-46
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[Title]
T-
cell
growth,
cell
surface organization, and the galectin-glycoprotein lattice.
Basal
, activation, and arrest signaling in T cells determines survival, coordinates responses to pathogens, and, when dysregulated, leads to loss of self-tolerance and autoimmunity.
At the T-
cell
surface, transmembrane glycoproteins interact with galectins via their N-glycans, forming a molecular lattice that regulates membrane localization, clustering, and endocytosis of surface receptors.
Galectin-T-
cell
receptor (TCR) binding prevents ligand-independent TCR signaling via Lck by blocking spontaneous clustering and CD4-Lck recruitment to TCR, and in turn F-actin transfer of TCR/CD4-Lck complexes to membrane microdomains.
Galectin also localizes the tyrosine phosphatase CD45 to microdomains and the immune synapse, suppressing
basal
and activation signaling by Lck.
Genetic and metabolic control of N-glycan branching co-regulate homeostatic set-points for
basal
, activation, and arrest signaling in T cells and, when disturbed, result in T-
cell hyperactivity
and autoimmunity.
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14672941.001
]
[Cites]
Annu Rev Immunol. 2004;22:531-62
[
15032588.001
]
[Cites]
Science. 2004 Oct 1;306(5693):120-4
[
15459394.001
]
(PMID = 19594640.001).
[ISSN]
1600-065X
[Journal-full-title]
Immunological reviews
[ISO-abbreviation]
Immunol. Rev.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI082266; United States / NIAID NIH HHS / AI / AI053331-06A1; United States / NIAID NIH HHS / AI / R01 AI053331-06A1; United States / NIAID NIH HHS / AI / R01 AI053331; United States / NIAID NIH HHS / AI / AI082266-01A2; United States / NIAID NIH HHS / AI / R01 AI082266-01A2
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Galectins; 0 / Glycoproteins; 0 / Receptors, Antigen, T-Cell; EC 2.- / Transferases; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 3.1.3.48 / Antigens, CD45
[Number-of-references]
105
[Other-IDs]
NLM/ NIHMS265770; NLM/ PMC3059806
25.
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
MedlinePlus Health Information.
consumer health - Memory
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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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
26.
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
27.
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.
Hazardous Substances Data Bank.
METHYLPHENIDATE
.
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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
28.
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
29.
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.
Hazardous Substances Data Bank.
MONOSODIUM GLUTAMATE
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
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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
30.
Curatolo P, D'Agati E, Moavero R:
The neurobiological basis of ADHD.
Ital J Pediatr
; 2010;36(1):79
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Attention-Deficit/
Hyperactivity
Disorder is not a single pathophysiological entity and appears to have a complex etiology.
Structural imaging studies show that brains of children with Attention-Deficit/
Hyperactivity
Disorder are significantly smaller than unaffected controls.
The prefrontal cortex,
basal
ganglia and cerebellum are differentially affected and evidence indicating reduced connectivity in white matter tracts in key brain areas is emerging.
Genetic, pharmacological, imaging, and animal models highlight the important role of dopamine dysregulation in the neurobiology of Attention-Deficit/
Hyperactivity
Disorder.
To date, stimulants are the most effective psychopharmacological treatments available for Attention-Deficit/
Hyperactivity
Disorder.
[MeSH-major]
Attention Deficit Disorder with
Hyperactivity
/ physiopathology. Brain / physiopathology
[MeSH-minor]
Animals. Atomoxetine Hydrochloride.
Basal
Ganglia / physiopathology. Behavior Therapy. Central Nervous System Stimulants / therapeutic use. Cerebellum / physiopathology. Dopamine / metabolism. Dopamine Agents / metabolism. Dopamine Uptake Inhibitors / therapeutic use. Drug Therapy, Combination. Evidence-Based Medicine. Humans. Italy. Methylphenidate / therapeutic use. Prefrontal Cortex / physiopathology. Propylamines / therapeutic use. Risk Factors. Treatment Outcome
MedlinePlus Health Information.
consumer health - Attention Deficit Hyperactivity Disorder
.
Hazardous Substances Data Bank.
METHYLPHENIDATE
.
Hazardous Substances Data Bank.
DOPAMINE
.
Hazardous Substances Data Bank.
ATOMOXETINE
.
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[ISSN]
1824-7288
[Journal-full-title]
Italian journal of pediatrics
[ISO-abbreviation]
Ital J Pediatr
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Central Nervous System Stimulants; 0 / Dopamine Agents; 0 / Dopamine Uptake Inhibitors; 0 / Propylamines; 207ZZ9QZ49 / Methylphenidate; 57WVB6I2W0 / Atomoxetine Hydrochloride; VTD58H1Z2X / Dopamine
[Other-IDs]
NLM/ PMC3016271
31.
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.
SciCrunch.
OMIM: Data: Gene Annotation
.
The Lens.
Cited by Patents in
.
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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
32.
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
33.
Sagi Y, Driguès N, Youdim MB:
The neurochemical and behavioral effects of the novel cholinesterase-monoamine oxidase inhibitor, ladostigil, in response to L-dopa and L-tryptophan, in rats.
Br J Pharmacol
; 2005 Oct;146(4):553-60
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In sharp contrast to the inductive effect of the MAO A/B inhibitor, tranylcypromine (TCP), on stereotyped
hyperactivity
in response to L-dopa (50 mg kg(-1)) or L-tryptophan (100 mg kg(-1)), ladostigil completely inhibited these behavioral
hyperactivity
syndromes.
Accordingly, acute rivastigmine (2 mg kg(-1)) and chronic TV3279 abolished the ability of TCP to initiate L-dopa-induced
hyperactivity
, while scopolamine (0.5 mg kg(-1)) reversed the inhibitory effect of chronic ladostigil on L-dopa-induced
hyperactivity
, suggesting that ladostigil may attenuate successive locomotion by activating central cholinergic muscarinic receptors.Finally, while chronic ladostigil administration to naïve rats resulted in preserved spontaneous motor behavior, acute treatment with ladostigil decreased motor performance, compared to control animals.
[MeSH-major]
Basal
Ganglia / drug effects. Behavior, Animal / drug effects. Cholinesterase Inhibitors / pharmacology. Hippocampus / drug effects. Hyperkinesis / prevention & control. Indans / pharmacology. Monoamine Oxidase Inhibitors / pharmacology. Motor Activity / drug effects
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[ISSN]
0007-1188
[Journal-full-title]
British journal of pharmacology
[ISO-abbreviation]
Br. J. Pharmacol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / (N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate; 0 / (N-propargyl-(3R) and (3S) aminoindan-5-yl)-ethyl methyl carbamate; 0 / Carbamates; 0 / Cholinesterase Inhibitors; 0 / Indans; 0 / Monoamine Oxidase Inhibitors; 0 / Muscarinic Antagonists; 0 / Phenylcarbamates; 333DO1RDJY / Serotonin; 3E3V44J4Z9 / Tranylcypromine; 451IFR0GXB / Scopolamine Hydrobromide; 46627O600J / Levodopa; 8DUH1N11BX / Tryptophan; PKI06M3IW0 / Rivastigmine; VTD58H1Z2X / Dopamine; X4W3ENH1CV / Norepinephrine
[Other-IDs]
NLM/ PMC1751181
34.
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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[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
35.
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
36.
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
37.
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
38.
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
39.
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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[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
40.
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
41.
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
Hazardous Substances Data Bank.
DOPAMINE
.
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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
42.
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
43.
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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HEROIN
.
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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
44.
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
MedlinePlus Health Information.
consumer health - Body Weight
.
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consumer health - Obesity
.
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Norepinephrine
.
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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
45.
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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[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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11320258.001
]
(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
46.
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
47.
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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[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
48.
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
49.
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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0918-9440
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Journal of plant research
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J. Plant Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
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Japan
50.
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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[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
[Chemical-registry-number]
0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Receptors, Immunologic
[Other-IDs]
NLM/ PMC2788702
51.
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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[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
52.
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
53.
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
54.
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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consumer health - Interstitial Cystitis
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(subscription/membership/fee required).
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[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
55.
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
56.
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
Pharmacogenomics Knowledge Base.
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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
57.
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).
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(PMID = 16923152.001).
[ISSN]
1601-1848
[Journal-full-title]
Genes, brain, and behavior
[ISO-abbreviation]<