Abstract

We examined the pharmacological basis for the suppression of the masseteric (jaw-closer) reflex which occurs during the behavioral state of active sleep. Accordingly, the masseteric reflex was recorded in intact, unanesthetized, normally respiring cats during naturally occurring states of wakefulness and active sleep. The amplitude of the reflex during these states was determined before and after strychine, picrotoxin, and bicuculline methiodide were applied, by microinjection, to the trigeminal motor nucleus. The effectiveness of each drug in blocking the active sleep-related suppression of the masseteric reflex was examined and compared with the degree of suppression evoked, during wakefulness, by stimulation of the inferior alveolar nerve. Microinjection of strychnine (50 μ M to 20 m M) reduced the degree of suppression of the masseteric reflex during active sleep, but was markedly more effective in blocking reflex suppression that was induced by stimulating the inferior alveolar nerve. Picrotoxin and bicuculline methiodide (10 μ M to 5 m M) produced a nonspecific increase in the amplitude of the masseteric reflex during both states. Thus, these substances did not appear to reduce the degree of reflex suppression induced by inferior alveolar nerve stimulation or that occurring spontaneously during active sleep. We concluded that strychnine-sensitive postsynaptic inhibition does participate in the suppression of masseter motor activity during active sleep, but that it is not the exclusive factor responsible for atonia of the masseter musculature during this state.

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