We have investigated the effects of systemic administration of two Symbol (NMDA) receptor antagonists and two opiate agonists on nociception during and after tail ischaemia in conscious rats. The two NMDA receptor antagonists, D-2-amino-5-phosphonovalerate (APV) and ketamine hydrochloride, did not alter tail flick latencies in rats not subjected to ischaemia but inhibited post-ischaemic hyperalgesia (PIH) in a dose-dependent manner. Neither of these agents impaired motor function of the rats, as assessed by rotarod performance, suggesting a purely sensory antinociceptive effect. The antinociceptive effect of APV during reperfusion following ischaemia was not antagonised by the μ-opiate receptor antagonist naloxone (1 mg/kg). The two opiate receptor agonists, morphine and pethidine, increased tail flick latencies in rats not subjected to ischaemia, inhibited PIH in a dose-dependent manner, and also caused significant motor malfunction, all in naloxone-reversible fashion. We conclude that the role of the NMDA receptor in mediating afferent nociceptive traffic is confined to its involvement in neuronal events mediating hyperalgesia.JOURNAL/jpain/04.02/00006396-199205000-00011/figure2-11/v/2017-07-22T040952Z/r/image-png
∗Correspondence to: Prof. D. Mitchell, Department of Physiology, University of the Witwatersrand Medical School, York Road, Parktown, 2193, Johannesburg, South Africa. Fax: 643-2765.
(Received 28 February 1990; revised 17 September 1991; accepted 19 September 1991.)
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