Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin

被引:17
|
作者
Powell, K. L. [1 ]
Kyi, M. [1 ]
Reid, C. A. [2 ]
Paradiso, L. [3 ]
D'Abaco, G. M. [3 ]
Kaye, A. H. [3 ]
Foote, S. J. [4 ,5 ]
O'Brien, T. J. [1 ,3 ]
机构
[1] Univ Melbourne, Dept Med, RMH WH, Melbourne, Vic 3050, Australia
[2] Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Melbourne, Vic 3050, Australia
[3] Univ Melbourne, Dept Surg, RMH WH, Melbourne, Vic 3050, Australia
[4] Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia
[5] Menzies Res Inst, Hobart, Tas, Australia
关键词
stargazin; absence epilepsy; animal models; GAERS; AMPA receptors; somatosensory cortex; thalamus;
D O I
10.1016/j.nbd.2008.04.012
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Stargazin is membrane bound protein involved in trafficking, synapse anchoring and biophysical modulation of AMPA receptors. A quantitative trait locus in chromosome 7 containing the stargazin gene has been identified as controlling the frequency and duration of absence seizures in the Genetic Absence Epilepsy Rats from Strasbourg (GAERS). Furthermore, mutations in this gene result in the Stargazer mouse that displays an absence epilepsy phenotype. GAERS stargazin mRNA expression is increased 1.8 fold in the somatosensory cortex and by 1.3 fold in the thalamus. The changes were present before and after the onset of absence seizures indicating that increases are not a secondary consequence of the seizures. Stargazin protein expression was also significantly increased in the somatosensory cortex after the onset of spontaneous seizures. The results are of significant importance beyond the GAERS model, as they are the first to show that an increase in stargazin expression may be pro-epileptic. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:261 / 265
页数:5
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