Actions of naloxone on spinal reflexes in 'acute spinal' cats

Naloxone HCl administered intravenously (0.1 to 2.0 mg/kg) increased polysynaptic reflexes and monosynaptic reflexes (MSR) in 'acute spinal' cats. The increase in reflex amplitude appears to result from a central action of the drug. It is not accompanied by an increase in the number of afferent fibers activated by the stimulus and it can be demonstrated in animals after all dorsal roots caudal to the spinal section have been cut. It is sometimes accompanied by a reduction in presynaptic or postsynaptic inhibition of the MSR. In these instances the effects on inhibition invariably can be reversed by reducing the amplitude of the MSR to predrug levels by decreasing the stimulus. Thus, the increased reflex produced by naloxone does not appear to be secondary to the blockade of inhibitory pathways. The actions of naloxone were not agnostic, since the administration of either morphine or oxymorphone routinely reduced the amplitude of all reflexes tested. Following the administration of a narcotic agonist, the administration of naloxone not only reversed the agonist induced depression, but superimposed on it the reflex augmentation observed in naive animals. These results are compatible either with the view that naloxone can act on a receptor other than the morphine receptor or that it is antagonizing an endogenous, morphine like substance.