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Vol. 298, Issue 2, 592-597, August 2001
Department of Anesthesiology, Medical College of Wisconsin,
Milwaukee, Wisconsin (M.O., H.M., M.N., J.P.K., L.F.T.); Department of
Toxicology, Hoshi University, Shinagawa-Ku, Japan (M.N.); and
Pharmaceutical Research Laboratory, Toray Industries Inc., Kamakura,
Japan (H.N.)
We have previously demonstrated that the antinociception induced
by either endomorphin-1 or endomorphin-2 given supraspinally is
mediated by the stimulation of µ-opioid receptors. However, the
antinociception induced by endomorphin-2 given supraspinally contains
additional components, which are mediated by the spinal release of
dynorphin A (1-17) acting on 
-opioid receptors and the spinal
release of [Met5]enkephalin acting on
2-opioid receptors in the spinal cord. The present
studies were performed to determine whether there are any differential
effects on the tail-flick inhibition induced by endomorphin-1 and
endomorphin-2 given intrathecally (i.t.) in mice. Endomorphin-1 or
endomorphin-2 given i.t. inhibited the tail-flick response in a
dose-dependent manner. The tail-flick inhibition induced by
endomorphin-1 was blocked by i.t. pretreatment with µ-opioid receptor
antagonist
D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 (CTOP), but not -opioid receptor antagonist nor-binaltorphimine (nor-BNI), 1-opioid receptor antagonist 7-benzylidene
naltrexamine (BNTX), or 2-opioid receptor antagonist
naltriben (NTB). In contrast, the tail-flick inhibition induced by
endomorphin-2 given i.t. was blocked by i.t. pretreatment with CTOP or
nor-BNI, but not BNTX or NTB. Intrathecal pretreatment with antiserum
against dynorphin A (1-17), but not antiserum against
[Met5]enkephalin, [Leu5]enkephalin, or
-endorphin, blocked the tail-flick inhibition induced by
i.t.-administered endomorphin-2. None of these antisera attenuated the
i.t.-administered endomorphin-1-induced tail-flick inhibition. It is
concluded that the tail-flick inhibition induced by endomorphin-1 and
endomorphin-2 given spinally is mediated by the stimulation of
µ-opioid receptors. However, the tail-flick inhibition induced by
spinally injected endomorphin-2 contains an additional component, which
is mediated by the spinal release of dynorphin A (1-17) acting on
-opioid receptors in the spinal cord. We propose that there are at
least two different subtypes of µ-opioid receptors for endomorphin-1
and endomorphin-2 to produce antinociception in the spinal cord.
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