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Remarkable alterations of Nav1.6 in reactive astrogliosis during epileptogenesis.

Abstract：

:Voltage-gated sodium channels (VGSCs) play a vital role in controlling neuronal excitability. Nav1.6 is the most abundantly expressed VGSCs subtype in the adult central nervous system and has been found to contribute to facilitate the hyperexcitability of neurons after electrical induction of status epilepticus (SE). To clarify the exact expression patterns of Nav1.6 during epileptogenesis, we examined the expression of Nav1.6 at protein and mRNA levels in two distinct animal models of temporal lobe epilepsy (TLE) including a post-SE model induced by kainic acid (KA) intrahippocampal injection and a kindling model evoked by pentylenetetrazole (PTZ). A prominent, seizure intensity-dependent increase of Nav1.6 expression in reactive astrocytes was observed in ipsilateral hippocampus of post-SE rats, reaching the peak at 21 days after SE, a time point during the latent stage of epileptogenesis. However, Nav1.6 with low expression level was selectively expressed in the hippocampal neurons rather than astrocytes in PTZ-kindled animals. This seizure-related increase of a VGSCs subtype in reactive astrocytes after SE may represent a new mechanism for signal communication between neuron and glia in the course of epileptogenesis, facilitating the neuronal hyperexcitability.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Zhu H,Zhao Y,Wu H,Jiang N,Wang Z,Lin W,Jin J,Ji Y

doi

10.1038/srep38108

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

38108

issn

2045-2322

pii

srep38108

journal_volume

6

pub_type

杂志文章

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