Previous studies have demonstrated that
generalized tonic-clonic seizures (GTCS) consisting of running/bouncing clonic and tonic extension can still be elicited in rats after brain transections which separate forebrain from brain stem, showing that forebrain circuitry is not required for GTCS. Inasmuch as sound-induced
generalized tonic-clonic seizures in rodents are characterized by running-bouncing clonic and tonic convulsions, we have hypothesized that these are brain stem
seizures that can occur independently of the forebrain. To test this hypothesis, we examined the response of two strains of genetically
epilepsy-prone rats (GEPR-3s and GEPR-9s) to seizure-evoking auditory stimuli 3 h after a precollicular transection or
sham surgery performed under
ether anesthesia. In addition, the effect of a precollicular transection on audiogenic
seizures was evaluated in normal rats made susceptible to such
seizures by infusing
NMDA into the inferior colliculus. Following the transection 58% of GEPR-9s displayed a sound-induced
tonic-clonic convulsion and the remaining 42% exhibited a sound-induced seizure when subjected to stimulation 5 min after a subconvulsant dose of
pentylenetetrazol (PTZ). While
sham surgery and the precollicular transection both reduced sound-induced seizure severity in GEPR-3s, the full seizure response could be elicited by sound stimulation following a subconvulsant dose of PTZ. Moreover, the audiogenic
seizures in normal rats rendered susceptible by
NMDA were unaltered by the precollicular transection. These findings show that the anatomical circuitry required for
generalized tonic-clonic seizures evoked by sound stimulation in rodents resides within the brain stem.