Synaptic changes in GABAA receptor expression in the thalamus of the stargazer mouse model of absence epilepsy

摘要: Absence seizures are known to result from disturbances within the cortico-thalamocortical network, which remains partially synchronous under normal conditions but switches a state of hypersynchronicity and hyperexcitability during absence seizures. There is evidence suggest that impaired GABAergic inhibitory function thalamus could contribute generation hypersynchronous oscillations in some animal models epilepsy. Recently, we demonstrated region-specific alterations tissue expression level GABAA receptors (GABA(A)Rs) α1 β2 subunits stargazer mouse model In present study investigated whether changes these also occur at synapses ventral posterior (VP) complex where they components phasic GABA(A)R receptors. Postembedding immunogold cytochemistry electron microscopy were used analyze relative synaptic VP thalamic region epileptic mice compared their non-epileptic littermates. We show there significant increase (53.6% 45.8%, respectively) stargazers, indicative an GABA(A)Rs thalamocortical (TC) relay neurons. Furthermore, α4 δ, constitute part tonic region, altered mouse. Semi-quantitative Western blotting showed δ thalamus, would indicate expression. Our findings levels both thalamus; inhibition be one many mechanisms contributing this model.