The role of the nucleus basalis of Meynert and reticular thalamic nucleus in pathogenesis of genetically determined absence epilepsy in rats: a lesion study.

The role of cholinergic nucleus basalis (of Meynert) and the reticular thalamic nucleus in mechanisms of the generation spontaneous spike-and-wave discharges (SWDs) was investigated in the WAG/Rij rat model of absence epilepsy. Selective lesions were affected by local unilateral intraparenchymal infusions of immunotoxin 192 IgG-saporin and cholinotoxin AF64A to the nucleus basalis and the rostral pole of reticular thalamic nucleus. Injections of 192 IgG-saporin into the nucleus basalis increased the number of spontaneous SWDs, while injections in the reticular thalamic nucleus were not effective. Thereby, a loss of cholinergic activity in the nucleus basalis stimulates the appearance of SWDs. At the same time, AF64A infused into reticular thalamic nucleus, besides the reduction of choline acetyltransferase immunoreactive neurons within contralateral nucleus basalis, produced some unspecified lesion of adjacent neuronal tissue, resulted in decrease of number and duration of SWDs as well as in spectral changes in EEG. Considering that the nucleus basalis is an important source of cortical and thalamic cholinergic afferentation, we conclude that cholinergic excitatory input from this structure is important in the control of SWDs in the WAG/Rij rat model of absence epilepsy.