Nociceptin (Orphanin FQ), an endogenous ligand for the ORL 1 receptor (opioid receptor-like 1 ), modulates responses of trigeminal neurons evoked by excitatory amino acids (EAA) and somatosensory stimuli. Wang, Xiao-Min, Kai Ming Zhang and Sukhbir S. Mokha. Department of Physiology, Meharry Medical College, 1005 D.B. Todd Blvd., Nashville, TN 37208, U.S.A.
APStracts 3:0175N, 1996.
SUMMARY AND CONCLUSIONS
1. This is the first in-vivo electrophysiological evidence demonstrating the effects of nociceptin (orphanin FQ), an endogenous ligand for the orphan receptor ORL 1 (opioid receptor-like 1 ), on nociceptive neurons in the central nervous system. The effects of nociceptin were tested on the responses of neurons recorded in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in the rat. 2. Nociceptin applied microiontophoretically produced a predominantly long lasting (5-30 min) inhibitory modulation of the N-methyl-D-aspartic acid (NMDA) - evoked responses of 24/31 nociceptive and 12/12 non-nociceptive neurons. Excitatory or biphasic effects of nociceptin were also observed in 6/43 neurons. Responses evoked by (+/-)-[alpha]-amino-3-hydroxy-5-methylisoxazole-4- propionic acid (AMPA) were reduced in 8/9 nociceptive and non-nociceptive neurons. 3. The inhibitory effect of nociceptin was not modality-specific, responses to both noxious and non-noxious stimuli were reduced. 4. Although naloxone applied iontophoretically blocked or reduced the peak inhibitory effect of DAMGO or U-50,488H, it did not produce a significant alteration in the peak inhibitory effect of nociceptin. 5. Nociceptin administered intracerebroventricularly (icv) produced a long lasting (20-35 min) reduction in the NMDA-evoked responses of 3/3 nociceptive neurons. 6. Nociceptin produces a predominantly antinociceptive action in the trigeminal system.

Received 18 July 1996; accepted in final form 21 August 1996.
APS Manuscript Number J572-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996