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Journal of Neuroscience, Vol 14, 5580-5589, Copyright © 1994 by Society for Neuroscience
Kappa 2 opioid receptors inhibit NMDA receptor-mediated synaptic currents in guinea pig CA3 pyramidal cells
RM Caudle, C Chavkin and R Dubner
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
The role of the endogenous opioid peptide dynorphin (1-17) in regulating
NMDA receptor-mediated synaptic currents was examined in guinea pig
hippocampus. Schaffer collateral/commissural fiber-evoked NMDA synaptic
currents were recorded using whole-cell patch-clamp techniques in CA3
pyramidal cells. Dynorphin was found to have dual effects on NMDA synaptic
currents, increasing currents at low concentrations and decreasing currents
at high concentrations. Only the inhibitory action of dynorphin was
sensitive to naloxone, indicating that this effect was mediated by an
opioid receptor. The inhibitory effect was mimicked by bremazocine, but not
by U69,593, U50,488, [D- Ala2, N-Me-Phe4, Gly-ol]-enkephalin, or
[D-Pen2,5]-enkephalin. Bremazocine's effect was blocked by naloxone, but
not by nor- binaltorphimine, cyprodime, or naltrindole. These findings
suggest that bremazocine's effect was mediated by the kappa 2 subtype of
opioid receptor. In addition, 1 microM naloxone and antisera to dynorphin
(1- 17) were found to increase NMDA-mediated synaptic currents. Nor-
binaltorphimine, cyprodime, naltrindole, and antisera to met-enkephalin did
not increase the NMDA synaptic current. These findings suggest that
endogenous dynorphin was acting at kappa 2 receptors to inhibit NMDA
receptor-mediated synaptic currents. Overall, these findings indicate that
dynorphin is an endogenous agonist for kappa 2 receptors in the CA3 region
of the guinea pig hippocampus and that these receptors regulate NMDA
receptor function.
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