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J Neurophysiol 78: 137-144, 1997;
0022-3077/97 $5.00
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The Journal of Neurophysiology Vol. 78 No. 1 July 1997, pp. 137-144
Copyright ©1997 The American Physiological Society

Dorsal Spinocerebellar Tract Neurons Are Not Subjected to Postsynaptic Inhibition During Carbachol-Induced Motor Inhibition

Ming-Chu Xi, Jack Yamuy, Rong-Huan Liu, Francisco R. Morales, and Michael H. Chase

Department of Physiology and the Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90024

Xi, Ming-Chu, Jack Yamuy, Rong-Huan Liu, Francisco R. Morales, and Michael H. Chase. Dorsal spinocerebellar tract neurons are not subjected to postsynaptic inhibition during carbachol-induced motor inhibition. J. Neurophysiol. 78: 137-144, 1997. Dorsal spinocerebellar tract (DSCT) neurons in Clarke's column in the lumbar spinal cord of cats anesthetized with alpha -chloralose were recorded intracellularly. The membrane potential activity and electrophysiological properties of these neurons were examined before and during the state of active-sleep-like motor inhibition induced by the injection of carbachol into the nucleus pontis oralis. The synaptic activity of DSCT neurons during carbachol-induced motor inhibition did not change compared with that during control conditions. In particular, there was an absence of inhibitory postsynaptic potentials (IPSPs) in high-gain recordings from DSCT neurons and the resting membrane potential of DSCT neurons was not significantly hyperpolarized during carbachol-induced motor inhibition. The mean amplitude of both monosynaptic excitatory postsynaptic potentials and disynaptic IPSPs evoked in DSCT neurons following stimulation of group I muscle afferents after the injection of carbachol was similar to that evoked before the injection of carbachol. There were no significant changes in the mean input resistance and membrane time constant of DSCT neurons during carbachol-induced motor inhibition. We conclude that, in contrast to lumbar motoneurons, DSCT neurons in Clarke's column are not postsynaptically inhibited during carbachol-induced motor inhibition. Therefore the population of spinal cord Ib interneurons that inhibit both DSCT neurons and lumbar motoneurons is not likely to be the interneurons that are responsible for the postsynaptic inhibition of motoneurons that occurs during carbachol-induced motor inhibition. The present findings also indicate that transmission through the DSCT is not modulated by postsynaptic inhibition at the level of DSCT neurons during carbachol-induced motor inhibition.




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