In this work, we have two goals: 1) to identify, at the single neuron level in the intact freely moving animal, the reticular cells mediating startle and 2) to test the hypothesis that the brainstem systems responsible for the inhibition of startle response are the same as those responsible for the nonspecific sensorimotor inhibition of REM sleep. In pursuit of these goals, we will investigate a group of medial pontine reticulospinal neurons which we believe have the response characteristics, projection pattern, an conduction velocity to mediate the startle response. This will be the first study of reticular cells during startle. We will similarly investigate a second group of cells, localized to the dorsolateral pons and medial medulla. These cells are maximally active in relation to the loss of muscle tone and sensory response in REM sleep, and in relation to certain waking movements. We will determine if these cells are active after stimuli that produce prepulse inhibition of startle and other conditions that reduce startle response amplitude. We will determine if lesions that block the sensorimotor inhibition of REM sleep also block prepulse inhibition of startle. We will investigate the neurochemical identify of pontomedullary mechanisms responsible for inhibition of startle, utilizing local infusion of blockers of cholinergic and glutaminergic transmission. We will determine the relation of the waking PGO spike to startle elicitation and inhibition. We will determine the effect of sleep-waking states and drowsiness on startle and its inhibition by prepulse stimulation. This work should produce a better understanding of the physiological and neurochemical mechanisms regulating startle. It should also elucidate the relation between the intensively investigated """"""""nonspecific' inhibitory phenomena accompanying REM sleep and the less well understood phenomena regulating startle response.
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