Effect of chronic morphine treatment on alpha(2)-adrenoceptor mediated autoinhibition of transmitter release from sympathetic varicosities of the mouse vas deferens

Karunanithi, Shanker and Lavidis, Nickolas A. (2001) Effect of chronic morphine treatment on alpha(2)-adrenoceptor mediated autoinhibition of transmitter release from sympathetic varicosities of the mouse vas deferens. British Journal of Pharmacology, 132 2: 403-410. doi:10.1038/sj.bjp.0703842


Author Karunanithi, Shanker
Lavidis, Nickolas A.
Title Effect of chronic morphine treatment on alpha(2)-adrenoceptor mediated autoinhibition of transmitter release from sympathetic varicosities of the mouse vas deferens
Formatted title
Effect of chronic morphine treatment on α2-adrenoceptor mediated autoinhibition of transmitter release from sympathetic varicosities of the mouse vas deferens
Journal name British Journal of Pharmacology   Check publisher's open access policy
ISSN 0007-1188
Publication date 2001
Sub-type Article (original research)
DOI 10.1038/sj.bjp.0703842
Volume 132
Issue 2
Start page 403
End page 410
Total pages 8
Editor R. A. North
Place of publication UK
Publisher Nature Publishing Group
Collection year 2001
Language eng
Subject C1
320701 Autonomic Nervous System
730104 Nervous system and disorders
Abstract 1 The effect of chronic morphine treatment (CMT) on sympathetic innervation of the mouse vas deferens and on alpha (2)-adrenoceptor mediated autoinhibition has been examined using intracellular recording of excitatory junction potentials (EJPs) and histochemistry. 2 In chronically saline treated (CST) preparations. morphine (1 muM) and the alpha (2)-adrenoceptor agonist (clonidine, 1 muM) decreased the mean amplitude of EJPs evoked with 0.03 Hz stimulation by 81+/-8% (n=16) and 92+/-6% (n=7) respectively. In CMT preparations, morphine (1 muM) and clonidine (1 muM) decreased mean EJP amplitude by 68+/-8% (n = 7) and 79+/-8% (n = 7) respectively. 3 When stimulating the sympathetic axons at 0.03 Hz. the mean EJP amplitude recorded from smooth muscles acutely withdrawn from CMT was four times greater than for CST smooth muscles (40.7+/-3.8 mV, n = 7 compared with 9.9+/-0.3 mV, n = 7). 4 Part of the increase in mean EJP amplitude following CMT was produced by a 31% increase in the density of sympathetic axons and varicosities innervating the smooth muscle. 5 Results from the present study indicate that the effectiveness of alpha (2)-adrenocrptor mediated autoinhibition is only slightly reduced in CMT preparations. Most of the cross tolerance which develops between morphine, clonidine and alpha (2)-adrenoceptor mediated autoinhibition occurs as a consequence of increased efficacy of neuromuscular transmission which is produced by an increase in the probability of transmitter release and an increase in the density of sympathetic innervation.
Keyword Pharmacology & Pharmacy
Alpha(2)-adrenoceptors
Morphine
Presynaptic
Withdrawal
Neurotransmission
Vas Deferens
Guinea-pig Ileum
External Calcium-concentration
Junction Potential Amplitude
Noradrenaline Release
Cross-tolerance
Neurotransmitter Release
Clonidine
Receptor
Rat
Alpha-2-adrenoceptors
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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Created: Tue, 14 Aug 2007, 16:47:09 EST