Origin and central pathways of crossed inhibitory effects of afferents from the masseteric muscle on the masseteric motoneuron of the cat

Abstract

Summary (1) Investigation was made of the origin of the masseteric group II afferents responsible for the crossed inhibition of the masseteric reflex and of the central pathways for these crossed effects. (2) The crossed inhibition evoked by stimulation of the masseteric nerve was abolished after selective section of non-spindle afferent fibers in the masseteric nerve. Stimulation of the trigeminal mesencephalic nucleus evoked a facilitation of the contralateral masseteric reflex. (3) The late phase of crossed inhibition of the masseteric reflex was abolished by transection of the brain stem at the obex level, leaving the early phase intact. The early phase was selectively blocked by a midline section of the brain stem at the level of the trigeminal motor nucleus. The early phase was blocked by strychnine, whereas the late phase was depressed by picrotoxin and augmented by pentobarbital. (4) The supratrigeminal inhibitory neurons were discharged by stimulation of the ipsilateral masseteric nerve. The time course and the intensity-response relation of the spike discharges correlated well with those of the early phase of masseterically evoked IPSPs in the masseteric motoneurons on both sides. The lingual and masseteric afferents made an excitatory convergence on the ipsilateral supratrigeminal neuron, but inhibited the contralateral supratrigeminal spike discharges. (5) It was concluded that the early phase of the masseterically induced crossed inhibition of the masseteric reflex was due to the group II afferents of non-spindle origin, and mediated by the commissural fibers which consisted of the axons of the supratrigeminal inhibitory neurons of the stimulated side to the contralateral masseteric motoneuron. Another conclusion was that the late phase was mediated by a polysynaptic route for which the structures caudal to the obex were indispensable.