Morphine–nicotine interaction in conditioned place preference in mice after chronic nicotine exposure
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...
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Published in | European journal of pharmacology Vol. 587; no. 1; pp. 169 - 174 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
10.06.2008
Elsevier |
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Abstract | 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. |
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AbstractList | 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. 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 micro-opioid receptors we used [3H]DAMGO autoradiography to study whether the number (B(max)) or affinity (K(D)) of mu-opioid receptors in the mouse brain are affected following chronic nicotine exposure. However, no changes were found in the number or affinity of micro-opioid receptors in any of the brain areas studied. Neither did we find alterations in the functional activity of mu-opioid receptors studied by [35S]GTPgammaS-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 micro-opioid receptors. |
Author | Piltonen, Marjo Vihavainen, Tanja Korpi, Esa R. Tuominen, Raimo K. Ahtee, Liisa |
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Keywords | [ 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 |
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SubjectTerms | [ 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 |
Title | Morphine–nicotine interaction in conditioned place preference in mice after chronic nicotine exposure |
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