The research described in this revised application is designed to utilize, for the first time, extracellular recording techniques in conjunction with procedures for drug microiontophoresis in the normally respiring cat to investigate the mechanism of suppression of trigeminal sensory neurons that was recently discovered to occur during naturally occurring behavioral states of active sleep. Detailed analyses will be performed of the antidromic spike wave form, spontaneous spike activity, glutamate-driven activity, and spike activity evoked by low-intensity stimuli applied to orofacial afferents of trigemino-thalamic tract neurons recorded during the states of wakefulness, quiet sleep, the non rapid-eye-movement and rapid-eye- movement episodes of active sleep. A interdigitated series of combined microiontophoretic and extracellular recording studies are proposed to investigate whether a process of postsynaptic inhibition or disfacilitation via depolarization of primary afferent terminals (PAD) accounts for the suppression of TGT neurons during active sleep; and whether glycine and/or GABA is the neurotransmitter responsible for mediating these phenomenon. The proposed studies will provide, in the chronic unanesthetized cat, l) a comprehensive description and quantitative analysis of the basic electrophysiological characteristics of individual trigemino-thalamic tract neurons during sleep and wakefulness and, 2) a normative find of information relating to the inhibitory control of trigeminal ascending sensory tract cells during different behavioral states. Such studies should provide important new insights into the normal functioning of the trigeminal system as a function of behavioral state and also provide a complimentary data base for that which already firmly exists for the state-dependent control of somatomotor outflow.
