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First published online on July 14, 2004.
 Copyright © 2004 by The Physiological Society
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jphysiol.2004.066159v1
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Received April 13, 2004
Revised May 10, 2004
Accepted after revision July 8, 2004

Dendritically released transmitters cooperate via autocrine and retrograde actions to inhibit afferent excitation

Michiru Hirasawa1, Yannick Schwab1, Sirajedin Natah1, Cecilia J. Hillard2, Ken Mackie3, Keith A. Sharkey1, and Quentin J. Pittman1*

1 University of Calgary
2 Medical College of Wisconsin
3 University of Washington

* To whom correspondence should be addressed. E-mail: pittman{at}ucalgary.ca.

Oxytocin is released from supraoptic magnocellular neurons and is thought to act at presynaptic receptors to inhibit transmitter release. We now show that this effect is mediated by endocannabinoids, but that oxytocin nonetheless plays an important role in endocannabinoid signaling. WIN55,212-2, a cannabinoid receptor agonist, mimicked the action of oxytocin and occluded oxytocin-induced presynaptic inhibition. The cannabinoid action is at the presynaptic terminal as shown by alteration in paired pulse ratio, a reduction in miniature EPSC frequency and immunohistochemical localization of CB1 receptors on presynaptic terminals. AM251, a CB1 receptor antagonist, blocked both the WIN55,212-2 and the oxytocin-induced presynaptic inhibition of EPSCs. Depolarization of postsynaptic magnocellular neurons (which contain fatty acid amide hydrolase, a cannabinoid catabolic enzyme) caused a transient inhibition of EPSCS that could be blocked by both the AM251 and Manning Compound, an oxytocin/vasopressin receptor antagonist. This indicates that somatodendritic peptide release and action on previously identified autoreceptors facilitates the release of endocannabinoids that act as mediators of presynaptic inhibition.


Key words: Cannabinoids • Oxytocin • Supraoptic nucleus




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