Neocortical and hippocampal EEG in rats during lateral hypothalamic lesion-induced hyperkinesia: relations to behavior and effects of atropine.

Rats received ferric ion depositing lateral hypothalamic lesions. Initially the lesions produced an area of cavitation surrounded by necrotic tissue. Subsequently, over 48 hr, this was surrounded by chromatolysis. Within 1 hr following lesioning and lasting for up to 8 hr the animals showed intense hyperkinesia, which consisted of stereotyped forward locomotion. The hyperkinesia was not blocked by atropine treatment. The atropine-resistant neocortical desynchronization and hippocampal RSA, which accompanies walking in normal rats, was absent in the hyperkinetic rats. The results suggest that hyperkinesia is produced by stimulation from lesion deposited Fe⁺⁺⁺ and may be related to the development of chromatolysis. The absence of normal forebrain EEG activity suggests that the stereotyped nature of the hyperkinesia may result from the absence of normal forebrain control over the motor systems for walking.