title: Systemic morphine selectively depresses a thalamic link of widespread nociceptive inputs in the rat.
abstract: The lateral part of the ventromedial thalamus (VM l) relays nociceptive inputs from the whole body surface to the dorsolateral frontal cortex. The aim of the present study was to investigate the effects of systemic morphine on nociceptive activity evoked in VM l neurones either by thermal (48 degrees C) or by supramaximal percutaneous electrical stimuli. The noxious thermal evoked responses were depressed by 10.8 +/- 10.1%, 48.3 +/- 23.0% and 67.3 +/- 10.1%, 5 min after i.v. injections of 1.0, 1.73 and 3.0 mg/kg of morphine, respectively. Moreover, strong depressive effects on the Adelta- and C-fibre responses were already present 5 min after the injection. The responses were significantly reduced by 7.2 +/- 5.9%, 32.5 +/ 11.1% and 37.2 +/- 11.8% for Adelta fibres after i.v. injections of 1.0, 1.73 and 3.0 mg/kg of morphine, respectively. The corresponding values for C-fibre evoked responses were 16.3 +/- 16.2%, 57.0 +/- 12.0% and 69.0 +/- 8.2%. The dose of morphine that reduced VM l neuronal nociceptive responses by 50% (1.73 mg/kg) was around 3.5 times lower than that necessary to inhibit the responses of its spinal or medullary relays under similar experimental conditions. These results, added to the data of the literature, suggest that supraspinal effects of morphine are primarily mediated at the thalamic level. It is tempting to speculate that morphine-induced reductions of attentional or psychomotor responses related to pain may be mediated by its action on VM l.
authors.affiliation: Physiopharmacologie du Système Nerveux, INSERM U-161, 2 rue d'Alésia, 75014 Paris, France. moncondl@broca.inserm.fr
authors.forename: Lénaïc
authors.initials: L
authors.lastname: Monconduit
authors.forename: Laurence
authors.initials: L
authors.lastname: Bourgeais
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Bernard
authors.forename: Luis
authors.initials: L
authors.lastname: Villanueva
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006930:Hyperalgesia / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009412:Nerve Fibers / Q000187:drug effects* / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000187:drug effects* / Q000502:physiology; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology; D010146:Pain / Q000188:drug therapy* / Q000503:physiopathology; D010812:Physical Stimulation; D017397:Prefrontal Cortex / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020651:Ventral Thalamic Nuclei / Q000187:drug effects* / Q000502:physiology
chemical_list: D000701:Analgesics, Opioid; D009292:Narcotic Antagonists; D009270:Naloxone; D009020:Morphine