KCa channels as therapeutic targets in episodic ataxia type-2
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Therapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug DiscoveryPrecision medicine in spinocerebellar ataxias: treatment based on common mechanisms of diseaseIntegration of modeling with experimental and clinical findings synthesizes and refines the central role of inositol 1,4,5-trisphosphate receptor 1 in spinocerebellar ataxiaThe riluzole derivative 2-amino-6-trifluoromethylthio-benzothiazole (SKA-19), a mixed KCa2 activator and NaV blocker, is a potent novel anticonvulsant.Major channels involved in neuropsychiatric disorders and therapeutic perspectivesPharmacological gating modulation of small- and intermediate-conductance Ca(2+)-activated K(+) channels (KCa2.x and KCa3.1)The first knockin mouse model of episodic ataxia type 2Flocculus Purkinje cell signals in mouse Cacna1a calcium channel mutants of escalating severity: an investigation of the role of firing irregularity in ataxia.4-aminopyridine does not enhance flocculus function in tottering, a mouse model of vestibulocerebellar dysfunction and ataxia.Ataxias and cerebellar dysfunction: involvement of synaptic plasticity deficits?Computational neurobiology is a useful tool in translational neurology: the example of ataxiaA randomized trial of 4-aminopyridine in EA2 and related familial episodic ataxiasDifferential cerebellar GABAA receptor expression in mice with mutations in CaV2.1 (P/Q-type) calcium channels.Mutation of plasma membrane Ca2+ ATPase isoform 3 in a family with X-linked congenital cerebellar ataxia impairs Ca2+ homeostasis.Chronic suppression of inositol 1,4,5-triphosphate receptor-mediated calcium signaling in cerebellar purkinje cells alleviates pathological phenotype in spinocerebellar ataxia 2 miceSelective positive modulator of calcium-activated potassium channels exerts beneficial effects in a mouse model of spinocerebellar ataxia type 2Pathogenesis of severe ataxia and tremor without the typical signs of neurodegeneration.Mitochondrial small conductance SK2 channels prevent glutamate-induced oxytosis and mitochondrial dysfunction.Iberiotoxin-sensitive and -insensitive BK currents in Purkinje neuron somataIn vivo analysis of cerebellar Purkinje cell activity in SCA2 transgenic mouse model.4-aminopyridine reverses ataxia and cerebellar firing deficiency in a mouse model of spinocerebellar ataxia type 6.The therapeutic potential of small-conductance KCa2 channels in neurodegenerative and psychiatric diseasesNew roles for the cerebellum in health and disease.K(Ca)2 channels: novel therapeutic targets for treating alcohol withdrawal and escalation of alcohol consumption.Update on the Pharmacotherapy of Cerebellar Ataxia and Nystagmus.Current Opinions and Areas of Consensus on the Role of the Cerebellum in Dystonia.Postnatal loss of P/Q-type channels confined to rhombic-lip-derived neurons alters synaptic transmission at the parallel fiber to purkinje cell synapse and replicates genomic Cacna1a mutation phenotype of ataxia and seizures in mice.Power Spectral Density Analysis of Purkinje Cell Tonic and Burst Firing Patterns From a Rat Model of Ataxia and Riluzole TreatedChlorzoxazone, an SK-type potassium channel activator used in humans, reduces excessive alcohol intake in rats.Small K channels: big targets for treating alcoholism?Computational insights into the neuroprotective action of riluzole on 3-acetylpyridine-induced ataxia in rats.The du(2J) mouse model of ataxia and absence epilepsy has deficient cannabinoid CB₁ receptor-mediated signalling.Structural insights into the potency of SK channel positive modulators.A new negative allosteric modulator, AP14145, for the study of small conductance calcium-activated potassium (KCa 2) channels.Ion channel dysfunction in cerebellar ataxia.Control of voluntary and optogenetically perturbed locomotion by spike rate and timing of neurons of the mouse cerebellar nuclei.Targeting potassium channels to treat cerebellar ataxia.Dendritic potassium channel dysfunction may contribute to dendrite degeneration in spinocerebellar ataxia type 1.A V-to-F substitution in SK2 channels causes Ca2+ hypersensitivity and improves locomotion in a C. elegans ALS model.Altered synaptic and firing properties of cerebellar Purkinje cells in a mouse model of ARSACS
P2860
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P2860
KCa channels as therapeutic targets in episodic ataxia type-2
description
2010 nî lūn-bûn
@nan
2010 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
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
KCa channels as therapeutic targets in episodic ataxia type-2
@ast
KCa channels as therapeutic targets in episodic ataxia type-2
@en
type
label
KCa channels as therapeutic targets in episodic ataxia type-2
@ast
KCa channels as therapeutic targets in episodic ataxia type-2
@en
prefLabel
KCa channels as therapeutic targets in episodic ataxia type-2
@ast
KCa channels as therapeutic targets in episodic ataxia type-2
@en
P2860
P1476
KCa channels as therapeutic targets in episodic ataxia type-2
@en
P2093
Kamran Khodakhah
Karina Alviña
P2860
P304
P356
10.1523/JNEUROSCI.6341-09.2010
P407
P577
2010-05-01T00:00:00Z