Effects of pentobarbitone and chlorpromazine on acoustically evoked potentials in the rat

Abstract

The effects of pentobarbitone and chlorpromazine on click-evoked potentials from the rat's auditory cortex, medial geniculate body, and hippocampus were investigated. Amplitude and latency measures made on sliding averages by a computer provided essentially continuous measurement of evoked responses throughout long experiments. Following a large dose of pentobarbitone (60 mg/kg) amplitudes of the several components of cortical responses displayed characteristic patterns of change that were readily apparent in the computer displays. Early deflections, for example, showed an initial rapid increase in amplitude, followed by a more gradual increase during deep anesthesia; they became suddenly very large at an early recovery stage and finally diminished slowly in a later recovery period. Late waves followed their own courses, were much reduced during deep anesthesia, and were generally large during late recovery periods when, however, they displayed large fluctuations in amplitude. In contrast, peak latencies of all components were increased in a relatively simple way. Early waves in medial geniculate body responses behaved like early cortical deflections, while late waves looked and behaved like hippocampal responses, disappearing during deep anesthesia. Chlorpromazine increased the amplitudes and latencies of all cortical deflections, while early medial geniculate body components showed similar, though smaller, changes. Waveforms of hippocampal responses were significantly modified by chlorpromazine, and peak latencies were increased, as they were at all sites.