Morphine–nicotine interaction in conditioned place preference in mice after chronic nicotine exposure

• Published in: European journal of pharmacology Vol. 587; no. 1; pp. 169 - 174
• Main Authors: Vihavainen, Tanja, Piltonen, Marjo, Tuominen, Raimo K., Korpi, Esa R., Ahtee, Liisa
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 10.06.2008; Elsevier
• Subjects: [ 35S]GTPγS; [ 3H]DAMGO; Analgesics, Opioid - pharmacology; Animals; Autoradiography; Biological and medical sciences; Conditioned place preference; Conditioning, Operant - drug effects; Cross-sensitization; Enkephalin, Ala-MePhe-Gly- - pharmacology; Guanosine 5'-O-(3-Thiotriphosphate) - pharmacology; Male; Medical sciences; Mice; Morphine; Morphine - pharmacology; Naltrexone - pharmacology; Narcotic Antagonists - pharmacology; Nicotine; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; Pharmacology. Drug treatments; Receptors, Opioid, mu - drug effects; [ 3H]DAMGO; [ 35S]GTPγS; Morphine; Conditioned place preference; Cross-sensitization; Nicotine; Interaction; Rodentia; Opiates; Narcotic analgesic; Nicotine;Morphine;Cross-sensitization;Conditioned place preference;[3H]DAMGO;[35S]GTPγS; Alkaloid; Vertebrata; Chronic; Mammalia; Mouse; Animal
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2008.03.028

Previously we found that morphine's effects on locomotor activity and brain dopamine metabolism were enhanced in mice after cessation of 7-week oral nicotine treatment. In the present experiments we show that such chronic nicotine exposure cross-sensitizes NMRI mice to the reinforcing effect of morphine in the conditioned place preference paradigm. The nicotine-treated mice developed conditioned place preference after being conditioned twice with morphine 5 mg/kg s.c. whereas in control mice a higher dose (10 mg/kg) of morphine was required. Since the reinforcing effect of morphine is mediated via µ-opioid receptors we used [ 3H]DAMGO autoradiography to study whether the number ( B max) or affinity ( K D) of µ-opioid receptors in the mouse brain are affected following chronic nicotine exposure. However, no changes were found in the number or affinity of µ-opioid receptors in any of the brain areas studied. Neither did we find alterations in the functional activity of µ-opioid receptors studied by [ 35S]GTPγS-binding. In conclusion, chronic oral nicotine treatment augments the reinforcing effects of morphine in mice, and this cross-sensitization does not seem to be mediated by µ-opioid receptors.