Abstract

The nature of the suppression of the masseteric monosynaptic reflex due to stimulation of the orbital gyrus was investigated by intracellular recording from massetteric motoneurons. The following results were obtained: (1) Either single pulses or pulse trains delivered to the orbital gyrus usually exerted a prolonged suppression (up to around 40 msec) of the masseteric monosynaptic reflex recorded along the masseteric nerve in response to stimulation of the trigeminal mesencephalic nucleus or the masseteric nerve itself. (2) The antidromic focal potential, recorded within the trigeminal motor nucleus in response to the stimulation of the masseteric nerve, was remarkably suppressed by stimulation of the orbital gyrus. (3) For intracellular studies, masseteric motoneurons were identified by anti-dromic spike potentials induced by stimulation of the masseteric nerve. Monosynaptic EPSPs were recorded in these masseteric motoneurons in response to stimulation of the trigeminal mesencephalic nucleus, confirming the monosynaptic excitatory linkage between the mesencephalic and the motor nucleus of the trigeminal nerve. (4) Stimulation of the orbital gyrus induced a prolonged hyperpolarizing potentials in masseteric motoneurons, the time course of which closely resembled that of the cortically induced suppression of the masseteric monosynaptic reflex. Monosynaptic, as well as antidromic, spikes of masseteric motoneurons were inhibited coincident with this hyperpolarizing potential. Hyperpolarization was changed to depolarization by the intracellular diffusion of Cl −. (5) Simultaneous recording of monosynaptic spikes in masseteric motoneurons and the masseteric reflex evoked by stimulation of the mesencephalic nucleus of V revealed a close temporal correlation between inhibition of the monosynaptic spikes and suppression of masseteric monosynaptic reflex. (6) It was concluded that an active postsyna[tic inhibition is primarily responsible for the observed suppression of the massteric monosynaptic reflex by electrical stimulation of the orbital gyrus.

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