Opioid tolerance and dependence in the magnocellular oxytocin system: a physiological mechanism?

Opioid tolerance and dependence in the magnocellular oxytocin system: a physiological mechanism? At the neurosecretory terminals in the neural lobe, oxytocin secretion is restrained by co‐secreted endogenous opioids, which act via kappa‐receptors. The co‐secreted opioids include products of pro‐dynorphin (released by both vasopressin and oxytocin terminals) and proenkephalin (released by oxytocin terminals). In morphine‐tolerant rats this opioid mechanism is more effective, but in late pregnancy it is less effective. Opioids also act directly on oxytocin cell bodies, via separate mu‐ and kappa‐receptors, inhibiting excitation by all stimuli tested, and also exert presynaptic and more distal actions on afferent systems. During chronic morphine exposure, tolerance and dependence develop in oxytocin neurones; the former involves reduction in mu‐opioid receptor density, while the latter may involve compensatory upregulation of mechanisms regulating Ca2+ influx. In mid‐pregnancy, the effectiveness of opioid mechanisms in the neural lobe increases, assisting the accumulation of oxytocin stores in advance of parturition, but by the end of pregnancy the effectiveness of these mechanisms is reduced. At this time, a separate endogenous opioid system, acting via mu‐receptors, actively restrains the electrical activity of oxytocin neurones. Release of this endogenous opioid inhibition may contribute to the increase in activity during parturition analogous to that occurring during morphine withdrawal excitation. Central opioid mechanisms retain the ability to control oxytocin neurones during parturition, and can interrupt established parturition by inhibiting oxytocin neurone firing rate in disadvantageous environmental circumstances. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Physiology Wiley

Opioid tolerance and dependence in the magnocellular oxytocin system: a physiological mechanism?

Experimental Physiology, Volume 80 (3) – May 1, 1995

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Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0958-0670
eISSN
1469-445X
DOI
10.1113/expphysiol.1995.sp003850
Publisher site
See Article on Publisher Site

Abstract

At the neurosecretory terminals in the neural lobe, oxytocin secretion is restrained by co‐secreted endogenous opioids, which act via kappa‐receptors. The co‐secreted opioids include products of pro‐dynorphin (released by both vasopressin and oxytocin terminals) and proenkephalin (released by oxytocin terminals). In morphine‐tolerant rats this opioid mechanism is more effective, but in late pregnancy it is less effective. Opioids also act directly on oxytocin cell bodies, via separate mu‐ and kappa‐receptors, inhibiting excitation by all stimuli tested, and also exert presynaptic and more distal actions on afferent systems. During chronic morphine exposure, tolerance and dependence develop in oxytocin neurones; the former involves reduction in mu‐opioid receptor density, while the latter may involve compensatory upregulation of mechanisms regulating Ca2+ influx. In mid‐pregnancy, the effectiveness of opioid mechanisms in the neural lobe increases, assisting the accumulation of oxytocin stores in advance of parturition, but by the end of pregnancy the effectiveness of these mechanisms is reduced. At this time, a separate endogenous opioid system, acting via mu‐receptors, actively restrains the electrical activity of oxytocin neurones. Release of this endogenous opioid inhibition may contribute to the increase in activity during parturition analogous to that occurring during morphine withdrawal excitation. Central opioid mechanisms retain the ability to control oxytocin neurones during parturition, and can interrupt established parturition by inhibiting oxytocin neurone firing rate in disadvantageous environmental circumstances.

Journal

Experimental PhysiologyWiley

Published: May 1, 1995

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