Abstract
The role of the lower brain stem in cortically induced alteration of somatic reflexes was investigated in the cat. The anterior portion of the orbital gyrus, previously implicated in the inhibition of monosynaptic and polysynaptic reflexes at all levels of the neuraxis, was shown to project directly to the ventromedial bulbar reticular formation (chiefly to the nucleus reticularis gigantocellularis) and to the pontine tegmentum (mainly to the nucleus reticularis pontis oralis). As a result of single pulse application to the anterior portion of the orbital gyrus, short latency (0.4–0.5 msec), direct responses were obtained in the ipsilateral and contralateral pontine and medullary reticular regions. The amplitude of these responses was approximately equal in the medullary inhibitory area, whereas, in the pontine facilitatory region, the size of contralaterally evoked responses was 40–65 % less than that of the ipsilaterally evoked potentials. The fact that the ventromedial bulbar reticular formation participates in the mechanism of orbital-cortically induced inhibition of the monosynaptic masseteric reflex, has been demonstrated in transection experiments. Transections of the medulla oblongata 2 mm caudal to the obex (P17) and lower had no effect on the efficiency of cortically induced reflex inhibition. More rostral transections (P15-P10) led to ineffectiveness and abolition of the cortically induced inhibitory influence. Moreover, transections at even more rostral levels (P8-P5) caused facilitation of the masseteric reflex following orbital-cortical stimulation. It is assumed that the descending orbito-medullary and orbito-pontine fibers synapse with neurons of the reticulo-spinal tract, and that axon collaterals of these neurons or axons of other reticular cells in the medullary or pontine reticular formation mediate inhibitory or excitatory influences, respectively, to the trigeminal and possibly also to other cranial nerve motor nuclei. A simple schematic drawing illustrates the role of the lower brain stem in orbital-cortically induced reflex alteration.
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