Postnatal expression of thalamic GABAA receptor subunits in the stargazer mouse model of absence epilepsy.

Abstract:

:Absence seizures are known to originate from disruptions within the corticothalamocortical network; however, the precise underlying cellular and molecular mechanisms that induce hypersynchronicity and hyperexcitability are debated and likely to be complex and multifactorial. Recent studies implicate impaired thalamic GABAergic inhibition as a common feature in multiple animal models of absence epilepsy, including the well-established stargazer mouse model. Recently, we demonstrated region-specific increases in the whole tissue and synaptic levels of GABAA receptor (GABAAR) subunits α1 and β2, within the ventral posterior region of the thalamus in adult epileptic stargazer mice compared with nonepileptic control littermates. The objective of this study was to investigate whether such changes in GABAAR subunits α1 and β2 can be observed before the initiation of seizures, which occur around postnatal (PN) days 16-18 in stargazers. Semiquantitative western blotting was used to analyze the relative tissue level expression of GABAAR α1 and β2 subunits in the thalamus of juvenile stargazer mice compared with their nonepileptic control littermates at three different time points before the initiation of seizures. We show that there is a statistically significant increase in the expression of α1 and β2 subunits in the thalamus of stargazer mice, at the PN7-9 stage, compared with the control littermates, but not at PN10-12 and PN13-15 stages. These results suggest that an aberrant expression of GABAAR subunits α1 and β2 in the stargazers does not occur immediately before seizure onset and therefore is unlikely to directly contribute to the initiation of absence seizures.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Seo S,Leitch B

doi

10.1097/WNR.0000000000000909

subject

Has Abstract

pub_date

2017-12-13 00:00:00

pages

1255-1260

issue

18

eissn

0959-4965

issn

1473-558X

journal_volume

28

pub_type

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