Effects of chlorpromazine on some motor reflexes

Abstract

The effects of chlorpromazine (CPZ) on the patellar reflex and segmentally evoked spinal cord potentials were determined in various cat preparations. CPZ in doses of 1–8 mg/kg given intravenously (as an accumulative dose) produced a significant depression of the patellar reflex and segmentally evoked potentials in animals with an intact central nervous system. Hypotension, potentiation of anesthesia, depression of nerve conduction in afferent and efferent nerves, an effect at the neuromuscular junction, or an effect directly on skeletal muscle or muscle spindle were ruled out as possible mechanisms of reflex depression. Studies in high spinal and decerebrate animals (Sherrington, Pollock-Davis) and decerebellate suggested a supraspinal sight of CPZ action. CPZ was shown to cause a significant depression of facilitation and inhibition of the patellar reflex produced by electrical stimulation of the mesencephalic facilitatory and medullary inhibitory areas of the reticular formation. The linguomandibular reflex (LMR) was also elicited in several preparations. This reflex was significantly depressed in intact and high spinal animals while the patellar reflex was depressed only in the former. CPZ-induced depression of segmentally evoked potentials was demonstrated to be dependent upon the intensity of electrical stimulation. CPZ was much less effective in depressing potentials elicited by supramaximal than by submaximal stimuli (80 per cent of maximum). The mean arterial blood pressure was depressed by CPZ in all preparations with an intact medullary vasomotor outflow. The site of CPZ depression of these motor reflexes is probably on neurons in portions of the bulbar facilitatory (BF) reticular area as well as a lesser depression of neurons in portions of the bulbar inhibitory reticular area. The possibility that CPZ may also act at a spinal level is discussed.