Drug-induced depression of gamma efferent activity—I. Peripheral reflexogenic effect of nicotine

Abstract

Nicotine in doses of 40–80 $\text{μg}\text{kg}$ i.v. was found to produce a generalized depression of spontaneous and reflexly-evoked γ efferent and attendant spindle afferent discharge in the cat under chloralose-urethane anesthesia. This depressant action was duplicated by sebacylcholine, a peripherally-acting nicotinic stimulant, and abolished by hexamethonium, a peripherally-acting nicotine antagonist. It was reduced or abolished by bilateral vagotomy. It is proposed that nicotine depresses γ activity by a reflex action arising from sensory receptors, a portion of which are within the vagal distribution. Small amounts of nicotine or sebacylcholine injected into the carotid sinus or into the lower aorta also affected y discharge. The γ depression produced by nicotine does not appear to be secondary to the blood pressure effects of the drug. The γ depression was preceded by an inconstant brief acceleration probably also of reflex origin. After spinal transection at C₁ the γ depressant effect of nicotine was abolished while the acceleratory response was still elicitable. The initiation of both reflex effects appears to be due to excitation by nicotine of cholinergic receptor sites at sensory terminals.