Electrophysiological evidence for nicotinic and muscarinic modulation of spinal cord reflexes

Abstract

Intravenous administration of physostigmine has been found to produce dose- and timedependent alterations of the lumbar monosynaptic and polysynaptic reflexes in spinal cats. A small dose of physostigmine (0.8 mg/kg) enhanced the monosynaptic reflex for 3 hr, while a larger dose (2.0 mg/kg) produced a pattern of initial depression which peaked at 5 min, followed by an increase which was maintained for 3 hr after injection. Both doses of physostigmine were found to produce a similar pattern of enhancement of the polysynaptic reflex. Atropine and mecamylamine antagonized the increase of the monosynaptic reflex produced by both doses of physostigmine. The initial depression of the monosynaptic reflex produced by the large dose of physostigmine was blocked by mecamylamine, but unaffected by atropine. The enhancement of the polysynaptic reflex, produced by both doses of physostigmine, was antagonized by atropine but not by mecamylamine. In addition, nicotine and oxotremorine were found to mimic the initial effects of physostigmine in the presence of the appropriate antagonist. These data show that both muscarinic and nicotinic receptors are involved differentially in the modulation of spinal reflexes and that physostigmine had an additional late effect which consistently occurred at 20 min after administration.