Thalamic mediodorsal and intralaminar nuclear lesions disrupt the generation of experimentally induced generalized absence-like seizures in rats.

The effect of bilateral electrolytic lesions of various thalamic sites on the generation of bilaterally synchronous spike and wave discharges (SWD) was studied in two experimental rat models of absence-like seizures. SWD induced by both pentylenetetrazole (20 mg/kg, i.p.) and gamma-hydroxybutyric acid (gamma-butyrolactone, 100 mg/kg, i.p.) were recorded simultaneously from the thalamus and cortex. In both models generation of SWD from the mediodorsal, intralaminar (central lateral and paracentral), ventroposterolateral (VPL) and the reticular thalamic (RT) nucleus was synchronous with that of frontoparietal cortex. Bilateral lesions in mediodorsal and intralaminar thalamic nuclei abolished SWD from both cortex and thalamus in both models. Similar lesions in VPL did not abolish, but attenuated the duration of pentylenetetrazole- and gamma-hydroxybutyric acid-induced SWD, more significantly from the thalamus than from the cortex. RT lesions were associated with more pronounced suppression of pentylenetetrazole-, but not gamma-hydroxybutyric acid-induced SWD in the thalamus. These findings suggest a potential role for mediodorsal and intralaminar thalamic nuclei in the generation of experimental absence-like seizures in rats.