Opioids modulate N -methyl- D -aspartic acid (NMDA)-evoked responses of
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.
SUMMARY AND CONCLUSIONS
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