Objective: This study tests the hypothesis that the ability of Hering’s nerve stimulation (HNS) to blunt seizure activity is dependent on the availability of dopamine in the amygdala. Methods: In 10 rats, Hering’s nerve (HN) on the right side was isolated and placed on an electrode and penicillin was locally placed on each rat’s left frontoparietal region to induce seizures. After the initiation of seizures, HN was stimulated. After the recurrence of seizure activity, the left basolateral amygdala was injected with 1.0 µl of normal saline, dopamine, haloperidol or 1% lidocaine in sequential tests. HN was stimulated after each injection and the latency and amplitude of the seizure activity were assessed. Results: Focal cortical penicillin induced seizures that resulted in tonic-clonic movement of the limbs and face that lasted 35–45 min. Tonic-clonic movements of the limbs and face of similar latency and amplitude were induced by repeated reapplication of penicillin in untreated rats. HNS decreased seizure activity, but infusion of haloperidol or lidocaine into the basolateral amygdala blocked this antiseizure effect of HNS. In contrast, infusion of saline or dopamine had no effect on the ability of HNS to blunt seizure activity. None of the amygdala injections altered the latency or amplitude of seizure activity. Conclusion: These results demonstrate that the ability of HNS to blunt seizure activity in the rat is dependent on an intact dopamine system in the basolateral amygdala. These data will hopefully be useful in furthering our understanding of the circuitry that allows peripheral nerve stimulation to alter seizure activity.
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