Neurophysiological studies of sensory gating in rats: Effects of amphetamine, phencyclidine, and haloperidol

Abstract

Central mechanisms of sensory gating were assessed in Sprague-Dawley rats by an evoked potential technique similar to one that we have previously used to show diminished sensory gating in psychotic patients. Middle latency (15–50 msec) auditory evoked potential responses were recorded at the skull in unanesthetized freely moving animals. Gating mechanisms were assessed in a conditioning-testing paradigm by measuring the supression of response to a 74 dB click test stimulus following an earlier identical conditioning stimulus at 0.5-sec intervals. The rats demonstrated significant suppression of the N50 response to the second auditory stimulus. Amphetamine treatment significantly interfered with the suppression of the response to the second stimulus; haloperidol, injected after the amphetamine, returned the conditioning-testing ratio toward normal values. Phencyclidine caused a similar decrease in suppression and was similarly antagonized by haloperidol. During some periods of hyperarousal, animals showed spontaneous loss of suppression; this condition could be reversed by haloperidol treatment. These results with psychotomimetic drugs in an animal model parallel abnormalities in sensory gating previously observed in psychotic human subjects.