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Vol. 294, Issue 3, 1106-1111, September 2000

Differential Mechanisms Mediating Descending Pain Controls for Antinociception Induced by Supraspinally Administered Endomorphin-1 and Endomorphin-2 in the Mouse1

Masahiro Ohsawa, Hirokazu Mizoguchi, Minoru Narita , Mei Chu, Hiroshi Nagase and Leon F. Tseng

Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin (M.O., H.M., M.N., M.C., L.F.T.); Department of Toxicology, Hoshi University, Shinagawa-Ku, Japan (M.N.); and Basic Research Laboratory, Toray Industries Inc., Kamakura, Japan (H.N.)

We have previously demonstrated that both endomorphin-1 and endomorphin-2 produce their antinociception by the stimulation of µ-opioid receptors. However, the antinociception induced by endomorphin-2 contains an additional component, which is mediated by the release of dynorphin A (1-17) acting on kappa -opioid receptors. These studies were done to determine whether the antinociception induced by endomorphin-1 and endomorphin-2 given supraspinally was mediated by the activation of different descending pain control pathways in the mouse. Specific receptor antagonists or antisera against endogenous opioid peptides were injected intrathecally to block the receptors or bind the released endogenous opioid peptides, and endomorphin-1 or endomorphin-2 was then administered i.c.v. to activate the descending pain control systems to produce antinociception. The tail-flick response was used as antinociceptive test. The blockade of the alpha 2-adrenoceptors and 5-hydroxytryptamine receptors in the spinal cord by i.t. injection of yohimbine and methysergide, respectively, inhibited the antinociception induced by i.c.v.-administered endomorphin-1 and endomorphin-2. However, the antinociception induced by endomorphin-2 was inhibited by i.t. pretreatment with delta 2-opioid receptor antagonist naltriben or kappa -opioid receptor antagonist nor-binaltorphimine, but not by the µ-opioid receptor antagonist D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 or the delta 1-opioid receptor antagonist 7-benzylidene naltrexamine. Intrathecal pretreatment with antiserum against Met-enkephalin attenuated the antinociception induced by i.c.v.-administered endomorphin-2, but not endomorphin-1. Furthermore, i.t. pretreatment with antiserum against dynorphin A (1-17) also inhibited the antinociception induced by i.c.v.-administered endomorphin-2, but not endomorphin-1. Intrathecal pretreatment with antiserum against Leu-enkephalin or beta -endorphin did not inhibit i.c.v.-administered endomorphin-1- or endomorphin-2-induced antinociception. The results indicate that, like other opioid µ-receptor agonists, morphine, and [D-Ala2,N-Me-Phe4, Gly5-ol]-enkephalin, endomorphin-1 and endomorphin-2 given i.c.v. produce antinociception by activating spinipetal noradrenergic and serotonergic pathways for producing antinociception. However, the antinociception induced by endomorphin-2 given i.c.v. also contains other components, which are mediated by the release of Met-enkephalin and dynorphin A (1-17) acting on opioid delta 2- and kappa -receptors, respectively, in the spinal cord.

1 This study was supported in part by Grant DA 03811 from the National Institutes of Health, National Institute on Drug Abuse (to L.F.T.). A preliminary report of some of these results was presented at the 29th Annual Meeting of the Society for Neuroscience, Miami, FL, October 23-28, 1999 (Tseng et al., 1999).

0022-3565/00/2943-1106$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


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