Titre : | Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common mu1 opioid receptor mechanism (1997) |
Auteurs : | TANDA G. ; F. E. PONTIERI ; DI CHIARA G. |
Type de document : | Article : Périodique |
Dans : | Science (Vol.276, n°5321, 27 June 1997) |
Article en page(s) : | 2048-2050 |
Langues: | Anglais |
Discipline : | PRO (Produits, mode d'action, méthode de dépistage / Substances, action mode, screening methods) |
Mots-clés : |
Thésaurus mots-clés NEUROBIOLOGIE ; PHARMACOLOGIE ; CANNABINOIDES ; TETRAHYDROCANNABINOL ; HEROINE ; DOPAMINE ; RECEPTEUR ; ANTAGONISTE ; MODELE ANIMAL |
Résumé : | The effects of the active ingredient of Cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), and of the highly addictive drug heroin on in vivo dopamine transmission in the nucleus accumbens were compared in Sprague-Dawley rats by brain microdialysis. Delta9-THC and heroin increased extracellular dopamine concentrations selectively in the shell of the nucleus accumbens; these effects were mimicked by the synthetic cannabinoid agonist WIN55212-2. SR141716A, an antagonist of central cannabinoid receptors, prevented the effects of Delta9-THC but not those of heroin. Naloxone, a generic opioid antagonist, administered systemically, or naloxonazine, an antagonist of micro1 opioid receptors, infused into the ventral tegmentum, prevented the action of cannabinoids and heroin on dopamine transmission. Thus, Delta9-THC and heroin exert similar effects on mesolimbic dopamine transmission through a common mu1 opioid receptor mechanism located in the ventral mesencephalic tegmentum. |
Domaine : | Drogues illicites / Illicit drugs |
Refs biblio. : | 22 |
Affiliation : | Dpt of Toxicology and Consiglio Nazionale delle Ricerche (CNR), Center for Neuropharmacology, Univ. of Cagliari, Cagliari, Italy |
Numéro Toxibase : | 1301000 |
Centre Emetteur : | 13 OFDT |
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