Abstract
This investigation was carried out to test the hypothesis that amygdaloid epileptiform activity is due to cholinergic hyperactivity. It was designed to study the underlying physiopathology of, and to act as an experimental model for, psychomotor epilepsy. Neostigmine was injected intracerebrally into the amygdala of the cebus monkey with chronically implanted "chemitrodes" fitted with EEG recording electrodes. The injections were made in the basal amygdaloid nucleus which normally shows very high acetylcholinesterase (AChE) enzymatic activity in histochemical preparations. Neostigmine injection resulted in very high amplitude spike activity in the amygdala only. Other brain areas, including the neighboring temporal cortex, did not show any marked EEG changes. In the first day or two, these EEG changes were associated with myoclonus localized in the ipsilateral muscles of facial expression and also associated with masticatory seizures. Subsequently the animal became aggressive and remained so several months after the injection of neostigmine. The EEG changes continued for approximately 6 weeks. Intramuscular injections of atropine diminished the amplitude of the epileptiform EEG discharges and modified slightly the animal's behavior.
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