The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 333-342
Copyright ©2000 by the American Physiological Society

Effect of Ethanol Upon Respiratory-Related Hypoglossal Nerve Output of Neonatal Rat Brain Stem Slices

Department of Physiology and Biophysics, School of Medicine, University of Washington, Seattle, Washington 98195-7290

Gibson, Ian C. and Albert J. Berger. Effect of Ethanol Upon Respiratory-Related Hypoglossal Nerve Output of Neonatal Rat Brain Stem Slices. J. Neurophysiol. 83: 333-342, 2000. The actions of ethanol (EtOH) on the respiratory output of the neonatal rat brain stem slice preparation in vitro are described. Ethanol inhibited respiratory-related hypoglossal nerve activity in a dose-dependent manner. The effect of EtOH was evident within 5 min and was reversible on EtOH washout. The actions of EtOH were qualitatively similar to those of two other alcohols, methanol and octanol. We investigated the dose-response relationship for each alcohol and determined that the order of potency was methanol < EtOH octanol, with EC₅₀ values of 291 mM, 39.7 mM, and 49.2 µM respectively. Application of either strychnine (5 µM) or bicuculline (5 µM) alone, partially but not significantly, reversed the inhibition of respiratory-related hypoglossal nerve activity produced by 50 mM EtOH. Preincubation of rhythmic slices with a combination of both strychnine and bicuculline (both 5 µM) partially, but significantly, blocked the inhibitory actions of EtOH, suggesting that other mechanisms also play a role in the action of EtOH. Preincubation of the slices with 25 µM APV reduced the relative degree of inhibition caused by EtOH suggesting that N-methyl-D-aspartate (NMDA)-receptor-mediated events can be affected by EtOH. Furthermore inhibition of protein kinase C by incubation with 100 nM staurosporine also reduced the efficacy of EtOH. These results suggest that the actions of EtOH may be mediated via glycine, GABA_A, and NMDA receptors and that activation of protein kinase C is involved in the EtOH-induced inhibition of respiratory-related hypoglossal nerve activity.