Abstract

Intravenous doses of 0.05–0.15 mg/kg of naloxone caused an increase in the spontaneous discharge rate of single dorsal horn units in lumbar spinal segments 5–7 in the spinal cat. This effect was seen with all of 21 units responding to noxious cutaneous stimulation. In contrast, the 7 units classified as non-nociceptive cutaneous were all unaffected by naloxone, even at doses of 0.4 mg/kg. Of two proprioceptive units, one was excited by naloxone. Naloxone also increased the response of nociceptive units to noxious radiant heat applied to the skin. Section of the ipsilateral dorsal roots of segments L 4-S 1 failed to abolish the excitatory effect of naloxone on the spontaneous activity of nociceptive units. Responses to naloxone were observed in laminae I, IV, V and VI. These results suggest that the effects of naloxone are not general and that nociceptive units in particular are excited. They also demonstrate that this effect occurs within the central nervous system and that its action is at the spinal level. It is suggested that the algesic effects of naloxone reported by others may be due, at least in part, to this action of naloxone in the spinal cord. While the results of this study support an hypothesis that an endogenous opioid agonist is being released continuously, and it is the prevention of the action of this endogenous substance on ‘opiate receptors’ at the spinal level which is observed as an excitation, it is also possible that naloxone may have an action at the spinal level independently of the actions of another agent, and that perhaps this action is on non-opiate receptors. A third possibility, raised from other recent work, is that the excitatory effects of naloxone may have been due to an antagonism of the effects of γ-aminobutyrate in the spinal cord.

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