The negative results in (3H)-spiperone binding suggest that changes in the serotonergic receptor in the frontal cortex and D2 receptors in the striatum does not participate the kindled seizure susceptibility.
In order to study the effects of antipsychotics on kindling process and the epileptic events, pharmacological action of antipsychotics on kindling process and the kindled convulsions, and changes in (3H)-spiperon binding following kindling were studied in this study. Following results were obtained: 1) Treatment with antipsychotics involving pimozide (0.4 mg/kg), haloperidol (0.4 mg/kg) and spiperone (0.5 mg/kg) facilitated the development of amygdaloid kindling. The number of daily stimulation required to induce the first generalized convulsion was: haloperidol group, 9.7; pimozide group, 11.5; spiperone group, 15.3 and the control group, 20.2. 2) While spiperone had weaker effect on kindling seizure development, it lowered the threshold stimulus intensity for inducing afterdischarge in the amygdaloid kindled seizure. The effect of spiperone to increase seizure susceptibility was dose dependent. In the temporal cortical kindled seizure, however, spiperone has no effect on the threshold intensity necessary to induce afterdischarge. 3) No change was found in (3H)-spiperone binding in the striatum, hippocampus and frontal cortex at one week after the final generalized convulsion, immediately after ceasing kindled generalized convulsion, there was no change in the (3H)-spiperone binding of the frontal cortex. It was suggested that antipsychotics facilitate the kindling seizure development and increase the amygdaloid kindled seizure susceptibility. The negative results in (3H)-spiperone binding suggest that changes in the serotonergic receptor in the frontal cortex and D2 receptor in the striatum does not participate the kindled seizure susceptibility.