title: Opioids modulate the calcitonin gene-related peptide8-37-mediated hindpaw withdrawal latency increase in thermally injured rats.
abstract: The present study was performed to explore the modulatory potential of different endogenous opioid systems on transmission of presumed nociceptive information at the spinal cord level in thermally injured rats. Thermal injury was performed by dipping the left paw into water 60 degrees C for 20 s. This induced a significant bilateral decrease in hindpaw withdrawal latency HWL to pressure. Intrathecal administration of 10 nmol of CGRP8-37 induced a significant bilateral increase in HWL in the thermally injured group and in the intact controls. The effect of different opioid receptor antagonists on the increased latency to withdrawal response induced by intrathecal injection of 10 nmol of CGRP8-37 was explored in the thermally injured rats. The effect was reversed by intrathecal injection of 40 and 80 nmol of: b-funaltrexamine (mu opioid receptor antagonist) and naltrindole (delta opioid receptor antagonist), but not by norbinaltorphimine (kappa opioid receptor antagonist). The results of the present study show that intrathecal CGRP8-37 increases hindpaw withdrawal latency in thermally injured rats, an effect reduced by a mu as well as by a delta opioid receptor antagonist.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
authors.forename: O
authors.initials: O
authors.lastname: Löfgren
authors.forename: L C
authors.initials: LC
authors.lastname: Yu
authors.forename: E
authors.initials: E
authors.lastname: Theodorsson
authors.forename: P
authors.initials: P
authors.lastname: Hansson
authors.forename: T
authors.initials: T
authors.lastname: Lundeberg
mesh_terms: D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects; D002056:Burns / Q000503:physiopathology*; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology*; D006614:Hindlimb; D007278:Injections, Spinal; D008297:Male; D008934:Mitogens / Q000494:pharmacology*; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D010446:Peptide Fragments / Q000494:pharmacology*; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D017465:Receptors, Opioid, delta / Q000037:antagonists & inhibitors; D017473:Receptors, Opioid, kappa / Q000037:antagonists & inhibitors; D017450:Receptors, Opioid, mu / Q000037:antagonists & inhibitors; D012018:Reflex / Q000187:drug effects* / Q000502:physiology
chemical_list: D008934:Mitogens; D009292:Narcotic Antagonists; D010446:Peptide Fragments; D017465:Receptors, Opioid, delta; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; C058636:calcitonin gene-related peptide (8-37); C051844:norbinaltorphimine; D009271:Naltrexone; C024524:beta-funaltrexamine; C055382:naltrindole; D015740:Calcitonin Gene-Related Peptide