Depression of α Motoneuron Activity by Excitation of Visceral Afferents in the Cardiopulmonary Region

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Abstract
The effect of vagal afferent firing, evoked by veratridine and phenyldiguanide, on the reflex responses of lumbosacral a motoneurons to muscle stretch (stretch reflex) and to electrical stimulation of muscle (monosynaptic reflex) and skin nerves (polysynaptic reflex) was investigated in cats under light chloralose-urethane anesthesia in the absence of fusimotor spindle feedback. It was found that α activity in ventral root filaments to both extensor and flexor muscles was depressed and that this depression was not only independent of the previously described γ effects but differed from them in various respects. Unlike the γ depression, α depression was infrequently preceded by an initial increase in activity. Thus, α depression often was already present when γ firing went through its early phase of acceleration. Furthermore, α depression was sometimes seen in the absence of γ effects. 5HT which had predominantly increased γ firing, produced a depression of α activity. Determination of the latent periods of the α depression and correlation of these with the latencies of the autonomic reflex responses, whose sites of initiation have provisionally been identified, prompt the conclusion that the viscerosomatic reflex elicited by phenyldiguanide arises from the pulmonary deflation receptors, while that elicited by veratridine originates in ventricular pressure and/or lung stretch receptors. The 5HT-induced α motor depression is of both vagal and non-vagal origin. It is proposed that these viscero-skeletomotor reflex effects constitute a mechanism which protects heart and lung from excessive demands of the body musculature.