Lesions producing REM sleep without atonia disinhibit the acoustic startle reflex without affecting prepulse inhibition.

This study determined whether the brainstem motor inhibition system that mediates muscle atonia during rapid eye movement (REM) sleep is involved in the elicitation and prepulse inhibition of the acoustic startle reflex. Electrolytic or neurotoxic (glutamate) lesions were made in the dorsolateral pontine tegmentum or the medial medulla, respectively, to produce the syndrome of REM sleep without atonia. Startle responses were released during REM sleep following the lesions. However, the amount of startle suppression produced by auditory prepulse after the lesion did not differ from that seen in intact controls. We conclude that REM sleep suppression of the acoustic startle responses is mediated by the system responsible for tonic motor inhibition, but auditory prepulse inhibition of the acoustic startle is not.