Neuronal parvalbumin and absence epilepsy in wag/rij rats

Abstract

In the WAG/Rij rat, a model for human absence epilepsy, spike-wave discharges and absence epileptic behaviour are fully symptomatic at an age of 6 months. The hypothesis is tested that the brain disorder underlying absence epilepsy is related to a changed distribution of neuronal parvalbumin (PV). Quantitative immunocytochemistry of PV shows that, in comparison to non-epileptic ACI control rats, the number of PV-containing neurons in WAG/Rij rats is considerably lower in the somatosensory cortex (parietal cortex area 1 and the forelimb area) and in the olfactory tubercle, but similar in the rostral reticular thalamic nucleus. The possible significance of the low amount of PV in the cortical areas in relation to absence epilepsy is discussed.