Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse

  title={Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by $\beta$-endorphin in pons/medulla of the $\mu$-opioid receptor knockout mouse},
  author={Hirokazu Mizoguchi and H.-e. Wu and Minoru Narita and F. Scott Hall and Ichiro Sora and George R. Uhl and Hiroshi Nagase and Leon F. Tseng},

Buprenorphine Blocks ϵ- and μ-Opioid Receptor-Mediated Antinociception in the Mouse

It is concluded that buprenorphine, at small doses, blocks ϵ-opioid receptor-mediated β-endorphin-induced antinociception and μ-opionceptor-mediated DAMGO-inducedAntagonistic properties, and at high doses produces a μ-OPioid receptors-mediated antinOCiception.

Differential mechanism of G-protein activation induced by endogenous mu-opioid peptides, endomorphin and beta-endorphin.

The subject of the present review is to focus on the differential mechanism underlying G-protein activation induced by these mu-opioid peptides using the [35S]GTPgammaS binding assay.

Non-opioid actions of opioid peptides.

In vivo and in vitro characterization of naltrindole-derived ligands at the κ-opioid receptor

Interestingly, while 5’-AMN and 5'-MABN were not κ-selective, both compounds did show significant antidepressant- and anxiolytic-like effects at 7–14 days post-injection in mice, contrary to the hypothesis.

Recent Advances in the Search for the -Opioidergic System

Findings indicate that EM-1 may produce its rewarding effect via MOP-Rs, and the aversive effect induced by EM-2 may be associated with the stimulation of the EM- 1-insensitive Mop-R subtype and necessarily activate an endogenous KOPergic system in the mouse brain.

β-Endorphin Mediates the Development and Instability of Atherosclerotic Plaques

This study provides the first evidence that β-endorphin contributes to the acceleration of the progression and instability of atheromatous plaques, and μ-opioid receptor antagonists may be useful for the prevention and treatment of atherosclerosis.



Differential antinociceptive effects of endomorphin-1 and endomorphin-2 in the mouse.

It is proposed that endomorphin-1 produces antinociception by stimulating one type of mu-opioid receptor, whereas endomorphicin-2 initially stimulates different mu-OPioid receptors, which subsequently induce the release of dynorphins that act on kappa-opIOid receptors to produce antinOCiception.

A potent and selective endogenous agonist for the µ-opiate receptor

The discovery and isolation from brain of a peptide, endomorphin-1 (Tyr-Pro-Trp-Phe-NH2), which has the highest specificity and affinity for the µ receptor of any endogenous substance so far described and they maybe natural ligands for this receptor.

Delta opioid modulation of the binding of guanosine-5'-O-(3-[35S]thio)triphosphate to NG108-15 cell membranes: characterization of agonist and inverse agonist effects.

The ability of the delta opioid agonist DPDPE to stimulate binding of the GTP analog guanosine-5'-O-(3-[35S]thio)triphosphate to pertussis toxin-sensitive G proteins has been characterized in membranes from NG108-15 mouse neuroblastoma X rat glioma cells.

Antagonist-induced up-regulation of the putative epsilon opioid receptor in rat brain: comparison with kappa, mu and delta opioid receptors.

It is reported that chronic treatment with the opiate antagonist naltrexone dramatically increases the number of non-mu, non-delta,non-kappa binding sites in rat brain, as well as theNumber of mu, delta and kappa receptors.

Modulation by mu-opioid agonists of guanosine-5'-O-(3-[35S]thio)triphosphate binding to membranes from human neuroblastoma SH-SY5Y cells.

The ability of mu-opioid agonists to activate G proteins has been demonstrated by studying the binding of the GTP analogue guanosine-5'-O-(3-[35S]thio)triphosphate ([35S]GTP gamma S) to membranes

Spinal analgesic actions of the new endogenous opioid peptides endomorphin‐1 and ‐2

It is concluded that the endomorphins are potent spinal antinociceptive and anti-allodynic agents and that they or related compounds may prove therapeutically useful as spinal analgesics.

Stimulation of guanosine-5'-O-(3-[35S]thio)triphosphate binding by endogenous opioids acting at a cloned mu receptor.

It was found that the Ki values closely matched the EC50 values for [35S]GTP gamma S binding stimulation, indicating that a large receptor reserve does not exist for the complete activation of G proteins in this system.