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[Title] Direct visualization of spruce budworm antifreeze protein interacting with ice crystals: basal plane affinity confers hyperactivity.

It has been proposed that the exceptional activity of these AFPs depends on their ability to prevent ice growth at the basal plane.

To test the hypothesis that the hyperactivity of sbwAFP results from direct affinity to the basal plane, we fluorescently tagged sbwAFP and visualized it on the surface of ice crystals using fluorescence microscopy.

SbwAFP accumulated at the six prism plane corners and the two basal planes of hexagonal ice crystals.

In contrast, fluorescently tagged fish type III AFP did not adhere to the basal planes of a single-crystal ice hemisphere.

When ice crystals were grown in the presence of a mixture of type III AFP and sbwAFP, a hybrid crystal shape was produced with sbwAFP bound to the basal planes of truncated bipyramidal crystals.

These observations are consistent with the blockage of c-axial growth of ice as a result of direct interaction of sbwAFP with the basal planes.

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(PMID = 18339740.001).

[ISSN] 1542-0086

[Journal-full-title] Biophysical journal

[ISO-abbreviation] Biophys. J.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antifreeze Proteins; 0 / Ice

[Other-IDs] NLM/ PMC2426666

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Subthalamic neurons coordinate basal ganglia function through differential neural pathways.

The subthalamic nucleus (STN) is a key component of basal ganglia circuitry that mediates a variety of motor functions.

The STN neurons send glutamatergic projections to the output structures of basal ganglia, including the substantia nigra pars reticulata (SNr) and the entopeduncular nucleus, and also innervate the globus pallidus (GP).

Here we performed conditional ablation of the STN neurons by using immunotoxin-mediated cell targeting.

Ablation of the STN neurons increased spontaneous movement and reduced hyperactivity in response to DA stimulation.

[MeSH-major] Basal Ganglia / physiology. Neurons / physiology. Subthalamic Nucleus / physiology

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(PMID = 16120775.001).

[ISSN] 1529-2401

[Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience

[ISO-abbreviation] J. Neurosci.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] VTD58H1Z2X / Dopamine

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Combined damage to entorhinal cortex and cholinergic basal forebrain neurons, two early neurodegenerative features accompanying Alzheimer's disease: effects on locomotor activity and memory functions in rats.

In Alzheimer's disease (AD), cognitive decline is linked to cholinergic dysfunctions in the basal forebrain (BF), although the earliest neuronal damage is described in the entorhinal cortex (EC).

Only rats with combined lesions showed diurnal and nocturnal hyperactivity.

[MeSH-minor] Analysis of Variance. Animals. Antibodies, Monoclonal. Behavior, Animal. Cell Count / methods. Choline O-Acetyltransferase / metabolism. Male. Maze Learning / physiology. N-Glycosyl Hydrolases. N-Methylaspartate. Psychomotor Performance / drug effects. Rats. Rats, Long-Evans. Ribosome Inactivating Proteins, Type 1

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(PMID = 16760925.001).

[ISSN] 0893-133X

[Journal-full-title] Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

[ISO-abbreviation] Neuropsychopharmacology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / 192 IgG-saporin; 0 / Antibodies, Monoclonal; 0 / Ribosome Inactivating Proteins, Type 1; 6384-92-5 / N-Methylaspartate; EC 2.3.1.6 / Choline O-Acetyltransferase; EC 3.2.2.- / N-Glycosyl Hydrolases; N9YNS0M02X / Acetylcholine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Deletion of RAGE causes hyperactivity and increased sensitivity to auditory stimuli in mice.

The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor that belongs to the immunoglobulin superfamily of cell surface receptors.

However, how RAGE influences gross behavioral activity patterns in basal condition has not been addressed to date.

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(PMID = 20016851.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Receptors, Immunologic

[Other-IDs] NLM/ PMC2788702

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[CommentOn] Behav Neurosci. 2008 Jun;122(3):491-7 [18513119.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A non-tumor suppressor role for basal p19ARF in maintaining nucleolar structure and function.

However, basal NPM and ARF proteins form nucleolar complexes whose functions remain unknown.

Nucleoli from Arf(-/)(-) cells displayed increased nucleolar area, suggesting that basal ARF might regulate key nucleolar functions.

Concordantly, ribosome biogenesis and protein synthesis were dramatically elevated in the absence of Arf, causing these cells to exhibit tremendous gains in protein amounts and increases in cell volume.

Postmitotic osteoclasts from Arf-null mice exhibited hyperactivity in vitro and in vivo, demonstrating a physiological function for basal ARF.

Thus, basal ARF proteins act as a monitor of steady-state ribosome biogenesis and growth independent of their ability to prevent unwarranted hyperproliferation.

[MeSH-major] Cell Nucleolus / ultrastructure. Cyclin-Dependent Kinase Inhibitor p16 / physiology. Nuclear Proteins / physiology

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(PMID = 18070929.001).

[ISSN] 1098-5549

[Journal-full-title] Molecular and cellular biology

[ISO-abbreviation] Mol. Cell. Biol.

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / R01 GM066032; United States / NIGMS NIH HHS / GM / GM066032

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Ribosomal; 0 / Nuclear Proteins; 0 / RNA, Ribosomal; 0 / Tumor Suppressor Proteins; 117896-08-9 / nucleophosmin

[Other-IDs] NLM/ PMC2223401

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Effects of gastric vagotomy on visceral cell proliferation induced by ventromedial hypothalamic lesions: role of vagal hyperactivity.

In rats, ventromedial hypothalamic (VMH) lesions induce cell proliferation in the visceral organs (stomach, small intestine, liver, and pancreas) due to hyperactivity of the vagus nerve.

To investigate the effects of selective gastric vagotomy on VMH lesion-induced cell proliferation and secretion of gastric acid, we assessed the mitotic index (the number of proliferating cell nuclear antigen (PCNA)-immunopositive cells per 1,000 cells in the gastric mucosal cell layer) and measured the volume of secreted basal gastric acid.

VMH lesions resulted in an increased mitotic index and thickness of the gastric mucosal cell layer and gave rise to the hypersecretion of gastric acid.

Selective gastric vagotomy restored these parameters to normal without affecting cell proliferation in other visceral organs.

These results suggest that VMH lesion-induced vagally mediated cell proliferation in the visceral organs is associated with hyperfunction in these organs, and VMH lesion-induced resistance to ethanol may be due to thickening of the gastric mucosal cell layer resulting from cell proliferation in the gastric mucosa-this in turn is due to hyperactivity of the vagus nerve.

[MeSH-major] Cell Proliferation. Gastric Mucosa. Vagotomy. Vagus Nerve / physiology. Ventromedial Hypothalamic Nucleus / pathology

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(PMID = 19455436.001).

[ISSN] 0895-8696

[Journal-full-title] Journal of molecular neuroscience : MN

[ISO-abbreviation] J. Mol. Neurosci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Lou/C obesity-resistant rat exhibits hyperactivity, hypermetabolism, alterations in white adipose tissue cellularity, and lipid tissue profiles.

Basal lipolysis and sensitivity to noradrenaline were similar; however, the responsiveness to noradrenaline was lower in adipocytes from Lou/C compared with that from Wistar rats.

[MeSH-minor] Animals. Cell Count. Fatty Acid Synthase, Type I / genetics. Fatty Acids / metabolism. Lipolysis / physiology. Lipoprotein Lipase / genetics. Male. Motor Activity / physiology. Norepinephrine / pharmacology. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Species Specificity. Stearoyl-CoA Desaturase / genetics. Stearoyl-CoA Desaturase / metabolism. Sympathetic Nervous System / physiology. Sympathomimetics / pharmacology

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(PMID = 18006635.001).

[ISSN] 0013-7227

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Fatty Acids; 0 / Sympathomimetics; EC 1.14.19.1 / Scd1 protein, mouse; EC 1.14.19.1 / Stearoyl-CoA Desaturase; EC 2.3.1.85 / Fatty Acid Synthase, Type I; EC 3.1.1.34 / Lipoprotein Lipase; X4W3ENH1CV / Norepinephrine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prolonged blockade of NMDA or mGluR5 glutamate receptors reduces nigrostriatal degeneration while inducing selective metabolic changes in the basal ganglia circuitry in a rodent model of Parkinson's disease.

The ionotropic, N-methyl-D-aspartate receptor antagonist MK-801 increased cell survival in the substantia nigra pars compacta (SNc) and corrected the metabolic hyperactivity (increased cytochrome oxidase activity) of the ipsilateral substantia nigra pars reticulata (SNr) associated with the lesion, but showed no effects on the 6-OHDA-induced hyperactivity of the subthalamic nucleus (STN).

As opposed to MK-801, MPEP abolished the STN metabolic hyperactivity associated with the nigrostriatal lesion, without affecting SNr activity.

Specific modulation of STN hyperactivity obtained with mGluR5 blockade may, therefore, open interesting perspectives for the use of this class of compounds in the treatment of Parkinson's disease.

[MeSH-minor] Animals. Cell Survival / drug effects. Cell Survival / physiology. Disease Models, Animal. Dizocilpine Maleate / pharmacology. Dizocilpine Maleate / therapeutic use. Electron Transport Complex IV / drug effects. Electron Transport Complex IV / metabolism. Energy Metabolism / drug effects. Energy Metabolism / physiology. Male. Nerve Degeneration / drug therapy. Nerve Degeneration / physiopathology. Nerve Degeneration / prevention & control. Neuroprotective Agents / pharmacology. Neuroprotective Agents / therapeutic use. Oxidopamine. Pyridines / pharmacology. Pyridines / therapeutic use. Rats. Rats, Sprague-Dawley. Receptor, Metabotropic Glutamate 5. Receptors, Metabotropic Glutamate / antagonists & inhibitors. Receptors, Metabotropic Glutamate / metabolism. Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors. Receptors, N-Methyl-D-Aspartate / metabolism. Subthalamic Nucleus / drug effects. Subthalamic Nucleus / metabolism. Subthalamic Nucleus / physiopathology

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(PMID = 16289868.001).

[ISSN] 0969-9961

[Journal-full-title] Neurobiology of disease

[ISO-abbreviation] Neurobiol. Dis.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 6-methyl-2-(phenylethynyl)pyridine; 0 / Excitatory Amino Acid Antagonists; 0 / Grm5 protein, rat; 0 / Neuroprotective Agents; 0 / Pyridines; 0 / Receptor, Metabotropic Glutamate 5; 0 / Receptors, Glutamate; 0 / Receptors, Metabotropic Glutamate; 0 / Receptors, N-Methyl-D-Aspartate; 6LR8C1B66Q / Dizocilpine Maleate; 8HW4YBZ748 / Oxidopamine; EC 1.9.3.1 / Electron Transport Complex IV

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Functional analysis of the roles of direct and indirect pathways by using immunotoxin-mediated cell targeting approach].

The neural circuit connecting the cerebral cortex and the basal ganglia mediates a variety of brain functions including voluntary movement, motor learning, and reinforcement learning.

The pathogenesis of certain neurological and neuropsychiatric diseases involves the dysfunction of these dopamin systems; some of these diseases include Parkinson's disease, schizophrenia, and attention deficit hyperactivity disorder.

Immunotoxin-mediated cell targeting is an approach employed in transgenic animals to eliminated specific neuronal types from a neuronal circuitry.

Here, we describe the use of immunotoxin-mediated cell targeting for studying the neural circuitry that underlies the motor behavior demonstrated in response to systemic dopamine stimulation; further, we propose the potential mechanism that controls direct and indirect striatal pathway-dependent behavior.

[MeSH-major] Basal Ganglia / physiology. Cerebral Cortex / physiology. Immunotoxins. Neural Pathways / physiology. Neurons / physiology

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(PMID = 19378811.001).

[ISSN] 1881-6096

[Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo

[ISO-abbreviation] Brain Nerve

[Language] jpn

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 0 / Immunotoxins; VTD58H1Z2X / Dopamine

[Number-of-references] 38

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

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(PMID = 21176172.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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. meta-databases - Pharmacogenomic Annotation 827857453 for PMID:20029387 [PharmGKB] .

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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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Dopamine neurotransmission controls motor and perseverative behavior, is mediated by protein phosphorylation, and may be perturbed in disorders of attention and hyperactivity.

Under basal conditions, CK1delta OE mice exhibited horizontal and vertical hyperactivity, reduced anxiety, and nesting behavior deficiencies.

All together, under basal conditions and in response to drug stimulation, the behavioral phenotype of CK1delta OE mice is reminiscent of the symptoms and drug responses observed in attention-deficit/hyperactivity disorder and therefore the CK1delta OE mice appear to be a model for this disorder.

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(PMID = 20145109.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NIDA NIH HHS / DA / P01 DA010044; United States / NIMH NIH HHS / MH / P01 MH040899; United States / NIDA NIH HHS / DA / DA10044

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Excitatory Amino Acid Antagonists; 0 / Receptors, Dopamine D1; 0 / Receptors, Dopamine D2; 207ZZ9QZ49 / Methylphenidate; 6LR8C1B66Q / Dizocilpine Maleate; CK833KGX7E / Amphetamine; EC 2.7.11.1 / Casein Kinase Idelta

[Other-IDs] NLM/ PMC2840146

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[MeSH-minor] 5' Flanking Region. Adult. Attention Deficit Disorder with Hyperactivity / metabolism. Basal Ganglia / metabolism. Base Sequence. Female. Gene Expression. Gene Frequency. Humans. Male. Molecular Sequence Data. Sequence Analysis, DNA. Sequence Homology, Nucleic Acid

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(PMID = 16710758.001).

[ISSN] 0272-4340

[Journal-full-title] Cellular and molecular neurobiology

[ISO-abbreviation] Cell. Mol. Neurobiol.

[Language] eng

[Grant] United States / NIDA NIH HHS / DA / DA 06227; United States / NIDA NIH HHS / DA / DA 7092-01; United States / NIDA NIH HHS / DA / DA00280; United States / NIDA NIH HHS / DA / DA09490-01

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Dopamine Plasma Membrane Transport Proteins; 0 / SLC6A3 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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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(PMID = 16086033.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In this study, we documented the relationship between carboplatin-induced hair cell degeneration and VCN plasticity in the chinchilla.

Unilateral application of carboplatin (5mg/ml) on the round window membrane resulted in massive hair cell loss.

Outer hair cell degeneration showed a pronounced basal-to-apical gradient while inner hair cell loss was more equally distributed throughout the cochlea.

In VCN, the high-frequency area dorsally showed slightly yet significantly stronger GAP-43 up-regulation than the low-frequency area ventrally, possibly reflecting the high-to-low frequency gradient of hair cell degeneration.

Alternatively, massive fiber growth may represent a deleterious process causing central hyperactivity that leads to loudness recruitment or tinnitus.

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(PMID = 19435600.001).

[ISSN] 1878-5891

[Journal-full-title] Hearing research

[ISO-abbreviation] Hear. Res.

[Language] ENG

[Grant] United States / NIDCD NIH HHS / DC / R01 DC006630; United States / NIDCD NIH HHS / DC / R01 DC006630-05; United States / NIDCD NIH HHS / DC / R01 DC06630

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / GAP-43 Protein; BG3F62OND5 / Carboplatin

[Other-IDs] NLM/ NIHMS139908; NLM/ PMC2777517

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We found that, in the bladders of WT mice, ERbeta is expressed in the basal cell layer of the urothelium.

The hyperactivity of T cells may be because of an imbalance between ERalpha and ERbeta signaling in female ERbeta(-/-) mice.

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(PMID = 17522255.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Estrogen Receptor beta; 0 / Glycosaminoglycans; 0 / glucosaminoglycans

[Other-IDs] NLM/ PMC1887607

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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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(PMID = 19414552.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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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(PMID = 18757368.001).

[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 / Insulin; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt

[Other-IDs] NLM/ PMC2662067

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The molecular motor dynein and its associated regulatory subunit dynactin have been implicated in several neurodegenerative conditions of the basal ganglia, such as Huntington's disease (HD) and Perry syndrome, an atypical Parkinson-like disease.

However, dynactin is also able to act independently of dynein, and there is currently no direct evidence linking dynein to basal ganglia degeneration.

These mice exhibited motor and behavioural abnormalities including hindlimb clasping, early muscle weakness, incoordination and hyperactivity.

Our study supports a role for dynein dysfunction in the pathogenesis of neurodegenerative disorders of the basal ganglia, such as Perry syndrome and HD.

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(PMID = 20807776.001).

[ISSN] 1460-2083

[Journal-full-title] Human molecular genetics

[ISO-abbreviation] Hum. Mol. Genet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Microtubule-Associated Proteins; 0 / Receptors, Dopamine D2; 144198-36-7 / dynactin; EC 3.6.4.2 / Dyneins; VTD58H1Z2X / Dopamine

[Other-IDs] NLM/ PMC3298848