• Mie Kajiwara, Risako Kato, Yoshiyuki Oi, and Masayuki Kobayashi.
• Department of Pharmacology, Nihon University School of Dentistry, Tokyo, Japan; Department of Anesthesiology, Nihon University School of Dentistry, Tokyo, Japan.
• J. Pharmacol. Sci. 2020 Mar 1; 142 (3): 83-92.

AbstractLittle is known about how propofol modulates the spike firing correlation between excitatory and inhibitory cortical neurons in vivo. We performed extracellular unit recordings from rat insular cortical neurons, and classified neurons with high spontaneous firing frequency, bursting, and short spike width as high frequency with bursting neurons (HFB; pseudo fast-spiking GABAergic neurons) and other neurons with low spontaneous firing frequency and no bursting were classified as non-HFB. Intravenous administration of propofol (12 mg/kg) from the caudal vein reduced the firing frequency of HFB, whereas propofol initially increased (within 30 s) and then decreased the firing frequency of non-HFB. Both HFB and non-HFB spontaneous action potential discharge was depressed by propofol with a greater depression seen for HFB. Cross-correlograms and auto-correlograms demonstrated propofol-induced increases in the ratio of the peak, which were mostly observed around 0-10 ms divided to baseline amplitude. The analysis of interspike intervals showed a decrease in spike firing at 20-100 Hz and a relative increase at 8-15 Hz. These results suggest that propofol induces a larger suppression of firing frequency in HFB and an enhancement of synchronized neural activities in the α frequency band in the cerebral cortex (192 words).Copyright © 2019 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

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