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Kappa-opioids decrease excitatory transmission in the dentate gyrus of the guinea pig hippocampus.

J J Wagner¹, R M Caudle, C Chavkin

¹Department of Pharmacology, University of Washington, Seattle 98195.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|January 1, 1992

Summary

Kappa 1-opioid receptors in the guinea pig hippocampus inhibit glutamate release from perforant path terminals. This suggests endogenous dynorphins may act as feedback inhibitors of excitatory input to the dentate gyrus.

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Area of Science:

Neuroscience
Pharmacology
Neurophysiology

Background:

Kappa 1-opioid receptors are present in the guinea pig hippocampus.
The precise function of these receptors in synaptic transmission within the dentate gyrus is not fully understood.

Purpose of the Study:

To investigate the localization and functional role of kappa 1-opioid receptors in the guinea pig dentate gyrus.
To determine the effect of kappa 1-receptor activation on synaptic transmission in this brain region.

Main Methods:

Autoradiography using selective and nonselective radioligands to map kappa 1-opioid binding sites.
Extracellular and intracellular recordings of dentate granule cell responses to assess electrophysiological effects.
Pharmacological manipulation with selective agonists and antagonists, including U69,593 and norbinaltorphimine.

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Main Results:

Kappa 1-opioid binding sites are localized in the molecular layer of the dentate gyrus.
Activation of kappa 1-receptors by U69,593 inhibited population spike amplitude and reduced glutamatergic EPSPs.
This inhibition was mediated by presynaptic action, reducing glutamate release from perforant path terminals.
Endogenous dynorphin B also inhibited the population spike response.

Conclusions:

Presynaptic kappa 1-receptor activation in the dentate gyrus inhibits glutamate release.
Endogenous dynorphins may function as feedback inhibitors of excitatory input to the dentate gyrus.
These findings elucidate a novel regulatory mechanism in hippocampal circuitry.