Abstract

The work of Walker, et al. (Brit. J. Pharmacol. 36: 19SP-199P, 1969: 38: 106-116, 1970) who showed that i.v. injections of para-methoxyphenylethylamine (PMPEA) into spinal cats anestlmetized with α-chloralose and Paralyzed with gallamine triethiodide cause increases in monosynaptic reflexes of both flexor and extensor motoneurons, has been confirmed in the present investigation. The action of PMPEA on the flexion reflex has been studied with the same preparation. The drug may cause an increase, a simple decrease or a decrease after a transient increase in the size of the flexion reflex. The actions of PMPEA on monosynaptic and flexion reflexes in unanesthetized preparations were similar to those in chloralose-anesthetized animals. PMPEA consistently depolarized the membrane potentials of motoneurons in the lumbar enlargement. The mean depolarization was 8.1 mV, and the time course of the depolarization was similar to the time courses of the reflex changes caused by PMPEA. Polysynaptic excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials recorded from motoneurons were reduced in amplitude during the action of PMPEA, and the time course of the reduction in each case was similar to the period during which the resting potential was depolarized and the reflexes altered by the drug. Amplitudes of monosynaptic EPSPs recorded from motoneurons were not changed in any consistent manner by PMPEA. it is concluded that the depolarization of motoneurons, coupled with the lack of change in amplitude of the monosynaptic EPSP, accounts for the increase in the monosynaptic reflex by PMPEA, whereas the reduction in polysynaptic EPSPs, in combination with the depolarization of motoneurons, accounts for the variable changes in the flexion reflex produced by this drug.