These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Differential antinociception induced by spinally administered endomorphin-1 and endomorphin-2 in the mouse.
    Author: Ohsawa M, Mizoguchi H, Narita M, Nagase H, Kampine JP, Tseng LF.
    Journal: J Pharmacol Exp Ther; 2001 Aug; 298(2):592-7. PubMed ID: 11454920.
    Abstract:
    We have previously demonstrated that the antinociception induced by either endomorphin-1 or endomorphin-2 given supraspinally is mediated by the stimulation of mu-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 kappa-opioid receptors and the spinal release of [Met5]enkephalin acting on delta2-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 mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 (CTOP), but not kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI), delta1-opioid receptor antagonist 7-benzylidene naltrexamine (BNTX), or delta2-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 beta-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 mu-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 kappa-opioid receptors in the spinal cord. We propose that there are at least two different subtypes of micro-opioid receptors for endomorphin-1 and endomorphin-2 to produce antinociception in the spinal cord.
    [Abstract] [Full Text] [Related] [New Search]