Oral reflexes were first extensively studied by Miller et al .(15) and sherrington(20. )In their studies, the natural and electrical stimulation was applied to the decerebrate cat, and several reflex movements were induced. They reported that single electrical shock applied to the lingual nerve caused opening of the mouth via reflex arc of the masticatory muscles(15) Anatomical studies have shown that the processes of trigeminal mesencephalic mucleus terrminate in the spindles of masticatory muscles and give collaterals to the massetric motoneurn(12,25). Functionally, these collaterals make monsynaptic and excitatory linkage with massetric motoneuron(11,13,17,25). Therefore, the massetric reflex is not only caused by massetric stretch but also elicited by stimulation of trigeminal mesencephalic nucleus(11). During the masticatory movement some highly coordinated relation which underlies between tongue and jaw to prevent the injury from each other must exist. In previous data, we kenw that activation of masseteric nerve induced a marked depression of linguo-hypoglossal reflex (18) and presynaptic inhibition of jaw-opening reflex(16). Recently, Goldberg (10) reported a profound suppression on masseteric monosynaptic reflex. However, the role of trigeminal spinal mucleus which is the most important neural linkage in masticatory movement has not been clarified. In this paper, we will describe the effects of trigeminal spinal nucleus on the masseteric monosynaptic reflex elucidated by electrophysiological and pharmacological observation
