Expression of pannexin1 in the CNS of adult mouse:: Cellular localization and effect of 4-aminopyridine-induced seizures

被引:62
作者
Zappala, A.
Cicero, D.
Serapide, M. F.
Paz, C.
Catania, M. V.
Falchi, M.
Parenti, R.
Panto, M. R.
La Delia, F.
Cicirata, F.
机构
[1] Univ Catania, Dept Physiol Sci, I-95125 Catania, Italy
[2] Inst Nacl Neurol & Neurocirugia MVS, Dept Neurofisiol, Mexico City 14269, DF, Mexico
[3] CNR, Inst Neurol Sci, Sect Catania, I-95123 Catania, Italy
[4] Ist Super Sanita, AIDS Natl Ctr, I-00161 Rome, Italy
关键词
pannexin; mouse; brain; neurons;
D O I
10.1016/j.neuroscience.2006.03.053
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The expression pattern of pannexin1, a gene coding for a protein that forms gap junction channels, was studied as both mRNA and protein in the CNS of adult mouse. Pannexin1 was widely expressed in the CNS by neuronal cell types but not glial cells, except for Bergmann glial cells of the cerebellar cortex. Cells positive to Ca-binding proteins, principally parvalbumin, but also calbindin and calretinin, as well as glutamate decarboxylase 67 kDa isoform, were pannexin1-positive. Pannexin1 labeling was found in cells which are known to exhibit spontaneous and synchronous discharge, such as neurons of the inferior olivary complex and the reticular thalamic nucleus, and also in neurons whose electrical activity is not coupled with neighboring cells, such as motoneurons of the spinal cord. The analysis of cellular localization showed puncta that surrounded cell bodies (e.g. the pyramidal cells of hippocampus) or restricted areas inside the cell bodies (e.g. the spinal motoneurons). In Bergmann glial cells the staining was present as fine grains that covered a large part of the cellular surface. Pannexin1 stained cells that previous studies have reported as expressing connexin36, another protein forming gap junction channels. Thus, it was possible that these two proteins could be integrated in the same functions. Since connexin36 expression levels change after seizures, we examined the expression of both pannexin1 and connexin36 in cerebral cortex, hippocampus, cerebellum and brain stem at different time intervals (2, 4 and 8 h) after i.p. injection of 4-aminopyridine, which resulted in systemic seizures. The only modification of the expression levels observed in this study concerned the progressive decrement of the connexin36 in the hippocampus, while pannexin1 expression was unchanged. This finding suggested that pannexin1 and connexin36 are involved in different functional roles or that they are expressed in different cell types and that only those expressing the Cx36 are induced to apoptosis by epileptic seizures. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:167 / 178
页数:12
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