Transient occlusion of rat carotid arteries decreases susceptibility to pilocarpine seizures.

Bilateral clamping of the carotid arteries (BCCA) for 24 min protects animals against convulsive effects of intraperitoneal injection of 300 mg/kg of pilocarpine when administered 14 days after surgery. Electrographic recordings from hippocampus, frontal cortex, striatum and substantia nigra demonstrate that (1) no spontaneous spiking activity is caused by the BCCA when observed for up to 10 days after surgery, (2) spiking activity can only be recorded in limbic structures but not in the frontal cortex after systemic administration of pilocarpine. These observations suggest that the propagation of seizure activity from subcortical limbic structures to the neocortex is affected by BCCA.