Does chronic halothane exposure alter brain electrical activity? Sensory evoked potentials recorded from cortex, diencephalon, and mesencephalon in freely behaving rats

The average accoustic evoked response (AAER) obtained from freely behaving rats implanted stereotaxically with permanent semimicroelectrodes was employed as an electrophysiological tool to investigate the effects of chronic halothane exposure (0.5%, 3 hr/day, 5 days/wk) on brain function. Recordings were obtained before and after halothane exposure from the nucleus parafasciculus thalami (PF), mesencephalic central gray (CG), ventromedial hypothalamus (VMH), and somatosensory cortex (SC). The AAER components P₂, N₂ and P₃ were consistently observed within and between animals before (control) and after intermittent halothane exposure for 28 and 56 days. Individual peak amplitudes were quantitated and compared to halothane-naive (control) values. The responses recorded from the PF showed a statistically significant increase in amplitude (P₂ and P₃ components) resulting from halothane exposure over 28 days and further significant increases after 56 days. The AAER obtained from the SC revealed a significant increase only in the N₂ component after both 28 and 56 days. In contrast, the CG recording was altered only after 56 days (increased N₂ and P₃) and the VMH AAER was not altered by chronic halothane exposure at all. A general increase in AAER amplitudes is thus seen in the PF, SC, and CG; however, the time course and individual components affected vary markedly. The conclusion is therefore drawn that chronic halothane exposure under the conditions of the present study has selectively modified the various brain nuclei examined. These data demonstrate a pronounced alteration of sensory evoked potentials following chronic exposure to subanesthetic concentrations of halothane.