Opioids modulate N -methyl- D -aspartic acid (NMDA)-evoked responses of trigeminothalamic neurons. Wang, Xiao-Min and Sukhbir S. Mokha. Department of Physiology, Meharry Medical College, 1005 D.B. Todd Boulevard, Nashville, TN 37208, U.S.A.
APStracts 3:0113N, 1996.
1. The present study investigated opioid-mediated modulation of N-methyl- D - aspartic acid (NMDA) - evoked responses of trigeminothalamic neurons in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in rats anesthetized with urethane. 2. Microiontophoretic application of NMDA activated 18 /19 trigeminothalamic neurons. Administration of [ D -Ala 2 , N -Me-Phe 4 ,Gly 5 -ol]-Enkephalin (DAMGO), a selective [mu] opioid receptor agonist, reduced the NMDA-evoked responses in 77% of trigeminothalamic neurons. [ D -Pen 2,5 ]-Enkephalin (DPDPE), a selective [delta] opioid receptor agonist, produced inhibition of NMDA-evoked responses in 36% of neurons. 3. We suggest that: 1) NMDA receptor activation excites trigeminothalamic nociceptive neurons and may, therefore, mediate nociceptive transmission in the medullary dorsal horn; and 2) the predominantly inhibitory modulation of NMDA receptor mediated responses of nociceptive trigeminothalamic neurons by activation of [mu] and [delta] opioid receptors may provide a neural mechanism for the antinociceptive actions of opioids.

Received 4 April 1996; accepted in final form 30 May 1996.
APS Manuscript Number J278-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 17 June 96