A bilaterally induced mechanical lesion of the midbrain was highly effective in abolishing the hindlimb extensor (HLE) component of the maximal electroshock seizures (MES) in rats. Although these lesions produced damage to a variety of midbrain structures, correlations between different lesion placements and effects in the MES test provided evidence that damage to superior cerebellar peduncle (PCS) and/or reticular formation (RF) was responsible for inhibition of hindlimb extension. Moreover, discretely placed electrolytic lesions disrupting either the PCS or the RF were found to abolish the hindlimb extensor component of the MES test. These findings are consistent with the work of other investigators showing that total cerebellectomy abolishes the HLE component of MES and suggest that activity in the cerebellum and the midbrain reticular formation plays a major role in regulating the tonic phase of electroshock induced seizures.

Midbrain tegmental lesions, which prevent the hindlimb extensor (HLE) component of maximal electroshock seizures (MES), were found to have no effect on the electroshock, flurothyl, or pentylenetetrazol (PTZ) seizures thresholds. However, these lesions were found to antagonize the HLE component of the maximal PTZ seizure, and to elevate the threshold for electroshock induced tonic flexion. These findings suggest that lesion of the midbrain tegmentum involving the superior cerebellar peduncle and/or the midbrain reticular formation antagonize the tonic component of generalized seizures, but have little or no effect on the clonic component.