Decreased viability and absence-like epilepsy in mice lacking or deficient in the GABAA receptor α1 subunit.
about
The developmental evolution of the seizure phenotype and cortical inhibition in mouse models of juvenile myoclonic epilepsy.The human epilepsy mutation GABRG2(Q390X) causes chronic subunit accumulation and neurodegenerationPhysiological bases of the K+ and the glutamate/GABA hypotheses of epilepsy.Animal models of absence epilepsies: what do they model and do sex and sex hormones matter?Combining valosin-containing protein (VCP) inhibition and suberanilohydroxamic acid (SAHA) treatment additively enhances the folding, trafficking, and function of epilepsy-associated γ-aminobutyric acid, type A (GABAA) receptorsLow brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's diseaseAltered intrathalamic GABAA neurotransmission in a mouse model of a human genetic absence epilepsy syndrome.Striatal GABAergic and cortical glutamatergic neurons mediate contrasting effects of cannabinoids on cortical network synchrony.Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.ErbB4 reduces synaptic GABAA currents independent of its receptor tyrosine kinase activity.Ion Channel Genes and Epilepsy: Functional Alteration, Pathogenic Potential, and Mechanism of Epilepsy.Differential molecular and behavioural alterations in mouse models of GABRG2 haploinsufficiency versus dominant negative mutations associated with human epilepsyHigh-amplitude theta wave bursts characterizing narcoleptic mice and patients are also produced by histamine deficiency in mice.Suppression of cortical seizures by optic stimulation of the reticular thalamus in PV-mhChR2-YFP BAC transgenic mice.Dynamics of sensorimotor cortex activation during absence and myoclonic seizures in a mouse model of juvenile myoclonic epilepsy.How deactivating an inhibitor causes absence epilepsy: validation of a noble lie.Single-cell genetic expression of mutant GABAA receptors causing Human genetic epilepsy alters dendritic spine and GABAergic bouton formation in a mutation-specific mannerIon Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies.Defects at the crossroads of GABAergic signaling in generalized genetic epilepsies.
P2860
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P2860
Decreased viability and absence-like epilepsy in mice lacking or deficient in the GABAA receptor α1 subunit.
description
2012 nî lūn-bûn
@nan
2012 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@ast
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@en
type
label
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@ast
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@en
prefLabel
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@ast
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@en
P2093
P2860
P1433
P1476
Decreased viability and absenc ...... the GABAA receptor α1 subunit.
@en
P2093
Fazal M Arain
Kelli L Boyd
Martin J Gallagher
P2860
P304
P356
10.1111/J.1528-1167.2012.03596.X
P577
2012-07-19T00:00:00Z