Action of nicotine on reflexes in spinal cats

Abstract

The effects of nicotine bitartrate on spinal reflexes were studied in cats with spinal section. Intravenous nicotine bitartrate routinely depressed monosynaptic reflexes. The depression of the monosynaptic reflex by nicotine can be blocked by raising the arterial blood pH either by hyperventilating the animal or by infusing sodium bicarbonate while maintaining end respiratory PCO 2 at 4%. The effect of pH on the nicotine response is not secondary to an increased monosynaptic reflex amplitude or to local vasoconstriction. Volleys in ipsilateral cutaneous afferents can also reduce nicotine-induced depression of the monosynaptic reflex. Intravenous nicotine bitartrate almost invariably caused an increase in the amplitude of the polysynaptic reflex, which was not dependent on nicotine's stimulation of peripheral afferent endings. One mechanism by which nicotine increased the polysynaptic reflex is presumed to be stimulation of Renshaw cells, since recurrent conditioning often yielded monosynaptic reflex inhibition accompanied by polysynaptic reflex augmentation. Nicotine effectively blocked recurrent inhibition, both during the period of reduction of the monosynaptic reflex and following the return of the reflex to within 10% of control levels. The block was also observed following doses of nicotine which had only minimal effects on the monosynaptic reflex. Doses of nicotine large enough to reduce the monosynaptic reflex to at least 25% of control produced a transient reversal of recurrent inhibition to recurrent facilitation, when the conditioning and testing motor nerves belonged to closely related muscles.