Deafferentation of the vestibular organ: Effects on atropine-resistant EEG in rats

Abstract

Cortical and hippocampal EEG patterns that persist after atropine sulfate administration are defined as atropine-resistant. In the rat, such patterns are movement-related, cortical low-voltage fast activity (LVFA) and movement-related, hippocampal rhythmic slow activity (RSA or “theta”). A close relationship exists between head movement and activation of atropine-resistant EEG. In the present study, we asked whether manipulation of vestibular sensory input would affect atropine-resistant EEG. To allow experimenter control, 6 vestibular-intact rats were made cataleptic with haloperidol and were then injected with atropine sulfate. Movement of the rats* heads by the experimenter (passive head movement) failed to activate atropine-resistant EEG. These animals were then rotated on a turntable. Such vestibular stimulation, the effectiveness of which was reflected by postrotatory ocular nystagmus, &lso failed to activate atropine-resistant EEG. These and 5 other rats were then subjected to surgical or chemical deafferentation of the labyrinth. They were tested for EEG atropine resistance before and after this surgery. Although atropine-resistant EEG patterns in response to active bodily movements still appeared after vestibular deafferentation, the frequency of hippocampal RSA during active movement was reduced with or without atropine. In contrast, &n atropine-sensitive component in the hippocampal EEG during immobility was not changed by vestibular deafferentation. We conclude that vestibular reafferent feedback is neither necessary nor sufficient for the atropine-resistant EEG, but that such feedback from active movement has a modulatory effect on hippocampal RSA. © 1989, Psychonomic Society, Inc.. All rights reserved.