Compensatory reduction of Cav3.1 expression in thalamocortical neurons of juvenile rats of WAG/Rij model of absence epilepsy

•We studied T-type Ca2+ channels in thalamocortical neurons of juvenile WAG/Rij rats.•Cav3-mediated current is weakened in absence-prone strain.•G and I isoforms of Cav3 are principal in laterodorsal nucleus of thalamus.•The expression level of Cav3.1 is decreased in absence-prone strain.•Reduced Cav3.1 could compensate for epilepsy progression in juvenile WAG/Rij rats. Absence seizures are the non-convulsive form of generalized epilepsy critically dependent on T-type calcium channels (Cav3) in thalamic neurons. In humans, absences accompany only childhood or adolescent epileptic syndromes—though in its polygenic rat models WAG/Rij and GAERS the opposite developmental pattern is observed. Hereby we address this issue by transcriptional and functional study of thalamic Cav3 in juvenile (i.e., free of seizures) rats of the absence-prone WAG/Rij strain and their coevals of the maternal Wistar strain. First, we measured the low voltage-activated (LVA) Ca2+ current in freshly isolated thalamocortical neurons from laterodorsal nucleus of thalamus. The difference between current densities in control (12.9±1.8pA/pF) and absence epilepsy (7.9±1.8pA/pF) groups reached ∼39%. Second, we assessed the contribution of different T-channel isoforms into the reduction of Cav3-mediated current in WAG/Rij juveniles by means of RT PCR. The expression of all three LVA calcium channels was revealed with the prevalence of G and I isoforms. The expression level of G isoform (Cav3.1) was 35% smaller in WAG/Rij strain if compared to the control animals while that of H and I isoforms (Cav3.2 and Cav3.3, respectively) remained stable. The weakened expression of Cav3.1 in juveniles of WAG/Rij rats could represent a compensatory mechanism determining the pattern of the age dependency in the disease manifestation by this model of absence epilepsy.