The Journal of Neurophysiology Vol. 78 No. 4 October 1997, pp. 2145-2155
Copyright ©1997 The American Physiological Society

Relationship Between Sensory Stimuli-Elicited IPSPs in Motoneurons and PGO Waves During Cholinergically Induced Muscle Atonia

Kristi A. Kohlmeier, Faustino López-Rodríguez, Francisco R. Morales, and Michael H. Chase

Department of Physiology, and the Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095

Kohlmeier, Kristi A., Faustino López-Rodríguez, Francisco R. Morales, and Michael H. Chase. Relationship between sensory stimuli-elicited IPSPs in motoneurons and PGO waves during cholinergically induced muscle atonia. J. Neurophysiol. 78: 2145-2155, 1997. Inhibitory postsynaptic potentials (IPSPs) can be produced in masseter motoneurons by sensory stimuli after the injection of carbachol into the nucleus pontis oralis (NPO) of -chloralose-anesthetized cats. We have postulated previously that these IPSPs, which are induced in masseter motoneurons by sensory stimuli, arise as the result of phasic activation of the motor inhibitory system that mediates atonia occurring spontaneously during active sleep. In the present study, we determined that sensory stimuli, which excite different sensory pathways, somatosensory and auditory, also elicit ponto-geniculo-occipital (PGO) waves during the carbachol-induced state. Because the elicitation of PGO waves has been hypothesized to be a central sign of activation of alerting mechanisms, we suggest that these stimuli also excite those CNS structures that are involved in the alerting network. The temporal association of the sensory stimuli-elicited IPSPs and PGO waves also was examined by correlating the intracellular response of masseter motoneurons and the extracellular response of lateral geniculate nuclei neurons to somatosensory and auditory stimuli. Sensory stimuli produced an IPSP that had a similar latency from the foot of the elicited PGO wave as that of spontaneously occurring motoneuron IPSPs and PGO waves that occur during both carbachol-induced muscle atonia and naturally occurring active sleep. In addition, the intensity of the stimulus necessary for elicitation of PGO waves was found to be lower than that required for the elicitation of IPSPs in motoneurons. Additionally, evoked responses in masseter motoneurons during the carbachol-induced state were graded in response to increases in stimulus intensity. The preceding data suggest that some type of processing of sensory input occurs such that only those stimuli that are capable of activating alerting mechanisms involved in the generation of PGO waves result in an increase in activity in the motor inhibitory system. We conclude that there may be a functional link between alerting mechanisms involved in the generation of PGO waves and the motor inhibitory system that generates IPSPs in motoneurons. This functional link may serve to preserve atonia, and thus the state of active sleep, from potentially disruptive PGO-related influences that, during other behavioral states, result in motor activation.

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