Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice. - Wikidata - awgldk - TriplyDB

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

http://www.wikidata.org/entity/Q30497725

about

Converging roles of ion channels, calcium, metabolic stress, and activity pattern of Substantia nigra dopaminergic neurons in health and Parkinson's disease Electrophysiological properties of embryonic stem cell-derived neurons Ionic currents influencing spontaneous firing and pacemaker frequency in dopamine neurons of the ventrolateral periaqueductal gray and dorsal raphe nucleus (vlPAG/DRN): A voltage-clamp and computational modelling study.Subcellular expression and neuroprotective effects of SK channels in human dopaminergic neurons CyPPA, a Positive SK3/SK2 Modulator, Reduces Activity of Dopaminergic Neurons, Inhibits Dopamine Release, and Counteracts Hyperdopaminergic Behaviors Induced by Methylphenidate.Selective positive modulator of calcium-activated potassium channels exerts beneficial effects in a mouse model of spinocerebellar ataxia type 2 Understanding the susceptibility of dopamine neurons to mitochondrial stressors in Parkinson's disease.Mitochondrial small conductance SK2 channels prevent glutamate-induced oxytosis and mitochondrial dysfunction.Dopaminergic expression of the Parkinsonian gene LRRK2-G2019S leads to non-autonomous visual neurodegeneration, accelerated by increased neural demands for energy.Abnormal Development of Glutamatergic Synapses Afferent to Dopaminergic Neurons of the Pink1(-/-) Mouse Model of Parkinson's Disease.Parkinson's disease mouse models in translational research.Molecular determinants of selective dopaminergic vulnerability in Parkinson's disease: an update.Calcium-activated SK channels control firing regularity by modulating sodium channel availability in midbrain dopamine neurons.The Epac-Phospholipase Cε Pathway Regulates Endocannabinoid Signaling and Cocaine-Induced Disinhibition of Ventral Tegmental Area Dopamine Neurons.Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.HCN2 channels in the ventral tegmental area regulate behavioral responses to chronic stress.Nesfatin-1 decreases excitability of dopaminergic neurons in the substantia nigra.TrkAIII signals endoplasmic reticulum stress to the mitochondria in neuroblastoma cells, resulting in glycolytic metabolic adaptation.HTRA2 variations in Taiwanese Parkinson's disease.

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P2860

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

http://www.wikidata.org/entity/Q30497725

description

2010 nî lūn-bûn

@nan

2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@ast

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@en

type

label

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

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Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@en

prefLabel

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@ast

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@en

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P1476

Hyperexcitable substantia nigra dopamine neurons in PINK1- and HtrA2/Omi-deficient mice.

@en

P2093

Antonios Dougalis

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Gillian A C Matthews

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Matthew W Bishop

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Nicholas W Wood

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Richard Festenstein

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Subhojit Chakraborty

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P2860

The mechanism of Ca2+ -dependent regulation of kinesin-mediated mitochondrial motility

PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons

PINK1 protein in normal human brain and Parkinson's disease

Ca(2+) transfer from the ER to mitochondria: when, how and why

Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration.

Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice

Loss of function mutations in the gene encoding Omi/HtrA2 in Parkinson's disease

Ionic mechanisms underlying autonomous action potential generation in the somata and dendrites of GABAergic substantia nigra pars reticulata neurons in vitro

Ca(2+)-activated K+ channels: molecular determinants and function of the SK family

'Rejuvenation' protects neurons in mouse models of Parkinson's disease

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3009-3020

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10.1152/JN.00466.2010

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6

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104

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substantia nigra

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