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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on November 12, 2004; DOI: 10.1124/jpet.104.076224

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Received for publication August 17, 2004.
Revised November 10, 2004.
Accepted for publication November 11, 2004.

Differential mechanisms of antianalgesia induced by endomorphin-1 and endomorphin-2 in the ventral periaqueductal gray of the rat

Maia Terashvili 1, Hsiang-en Wu 1, Randy J Leitermann 1, Han-Sen Sun 1, Andrew D Clithero 1, Leon F Tseng 1*

1 Medical College of Wisconsin

* Address correspondence to: E-mail: ltseng{at}post.its.mcw.edu

Abstract

The effects of pretreatment with endomorphin-1 (EM-1) and endomorphin-2 (EM-2) given into the ventral periaqueductal gray (vPAG) to induce antianalgesia against the tail-flick (TF) inhibition produced by morphine given into the vPAG were studied in rats. Pretreatment with EM-1 (3.5-28 nmol) given into vPAG for 45 min dose-dependently attenuated the TF inhibition produced by morphine (9 nmol) given into vPAG. Similarly, pretreatment with EM-2 (1.7-7.0 nmol) for 45 min also attenuated the TF inhibition induced by morphine. However, a high dose of EM-2 (14 nmol) did not attenuate the morphine-produced TF inhibition. The attenuation of morphine-produced TF inhibition induced by EM-2 or EM-1 pretreatment was blocked by pretreatment with µ opioid antagonist (-)-naloxone (55 pmol) but not non-opioid (+)-naloxone (55 pmol). However, pretreatment with a morphine-6{beta}-glucuronide sensitive µ-opioid receptor antagonist 3-methoxynaltrexone (6.4 pmol) selectively blocked EM-2-, but not EM-1-induced antianalgesia. Pretreatment with dynorphin A(1-17) antiserum reversed only EM-2-, but not EM-1-induced antianalgesia. Pretreatment with antiserum against {beta}-endorphin, [Met5]enkephalin, [Leu5]enkephalin, substance P or cholecystokinin, or with {delta}-opioid receptor antagonist naltrindole (2.2 nmol) or {kappa}-opioid receptor antagonist norbinaltorphimine (6.6 nmol) did not affect EM-2-induced antianalgesia. It is concluded that EM-2 selectively releases dynorphin A(1-17) by stimulation of a novel subtype of µ-opioid receptor, tentatively designated as µ3 in the vPAG to induce antianalgesia, while the antianalgesia induced by EM-1 is mediated by the stimulation of another subtype of µ1 or µ2-opioid receptor.


Key words: Analgesia, Antianalgesia, Brain, Endomorphins, Opioid, rat


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J. Pharmacol. Exp. Ther., September 1, 2005; 314(3): 1101 - 1108.
[Abstract] [Full Text] [PDF]


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