dextro-Naloxone or levo-naloxone reverses the attenuation of morphine antinociception induced by lipopolysaccharide in the mouse spinal cord via a non-opioid mechanism.

Glial stimulation by intrathecal injection of lipopolysaccharide (LPS) attenuated the tail-flick inhibition produced by morphine given intrathecally in the spinal cord of the male CD-1 mice. The phenomenon has been defined as antianalgesia. The effects of dextro-naloxone or levo-naloxone on the attenuation of morphine-produced tail-flick inhibition induced by LPS were then studied.

p38 mitogen-activated protein kinase inhibitor SB203580 reverses the antianalgesia induced by dextro-morphine or morphine in the mouse spinal cord.

We have previously demonstrated that intrathecal pretreatment with dextro-morphine or morphine attenuates the morphine-produced antinociception. The phenomenon has been defined as antianalgesia, which is mediated by a non-opioid receptor [Wu, H., Thompson, J.

dextro- and levo-morphine attenuate opioid delta and kappa receptor agonist produced analgesia in mu-opioid receptor knockout mice.

We have demonstrated that the antianalgesia induced by dextro-morphine and levo-morphine is not mediated by the stimulation of mu-opioid receptors in male CD-1 mice. We now report that the dextro-morphine and levo-morphine attenuated antinociception produced by delta-opioid receptor agonist deltorphin II and kappa-opioid receptor agonist U50,488H given spinally in the male mu-opioid receptor knockout mice. The tail-flick response was used for the antinociceptive test.

Antianalgesia: stereoselective action of dextro-morphine over levo-morphine on glia in the mouse spinal cord.

We have previously shown that the naturally occurring levo-morphine at a subanalgesic picomolar dose pretreated i.t. induces antianalgesia against levo-morphine-produced antinociception.

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

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.

Nonopioidergic mechanism mediating morphine-induced antianalgesia in the mouse spinal cord.

Intrathecal (i.t.) pretreatment with a low dose (0.

Dynorphinergic mechanism mediating endomorphin-2-induced antianalgesia in the mouse spinal cord.

We have previously demonstrated that both endomorphin-1 (EM-1) and endomorphin-2 (EM-2) at high doses (1.75-35 nmol) given intrathecally (i.t.

Antinociceptive properties of oxymorphazole in the mouse.

Oxymorphazole (17-methyl-6,7-dehydro-3,14-dihydroxy-4,5 alpha-epoxy-6,7:3',4'-pyrazolomorphinan), a hydrophilic opioid, given intracerebroventricularly (2.5-50 nmol) or intrathecally (0.3-5 nmol) dose-dependently produced tail-flick inhibition in male CD-1 mice.