Inferior collicular interactions with limbic seizure activity.

Because under certain conditions, seizure activity electrically elicited from layers III and IV of the inferior collicular cortex can spread into forebrain regions, potential inferior collicular interactions with the amygdala were studied. Following acute electrical initiation of seizure activity from the inferior colliculus, no changes in amygdala EEG activity were noted. Following repetitive stimulation of the inferior colliculus, however, postictal spiking activity was noted in the amygdala, similar to interictal spiking reported for amygdala kindling, but this abnormal EEG activity did not coincide with any observable behavioral change. Conversely, the course of amygdala kindling in animals previously stimulated in the inferior colliculus progressed quite differently in comparison to control animals. Those animals repetitively stimulated in the inferior colliculus required a significantly greater number of amygdala kindling stimulations to reach class 5 seizure activity than did animals that received no inferior collicular stimulation and, unlike the controls, the chronic inferior collicular stimulation group usually regressed to class 2 or 3 seizure activity after the first class 5 seizure. Furthermore, the chronic inferior collicular stimulation group all exhibited wet-dog shakes during the amygdaloid kindling stimulation, whereas at no time did controls exhibit wet-dog shake behaviors. Finally, the seizure generalization from the inferior colliculus appears to be mediated by a mechanism distinct from the acute seizure activity, because a dose of diazepam (0.4 mg/kg), or carbamazepine (10 mg/kg), which had no effect on the wild running seizure, blocked behaviors indicative of seizure generalization. The significance of these results to epilepsy is discussed.