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 inEuropean 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
LanguageEnglish
Published Amsterdam 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.
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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Snippet 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...
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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
URI https://dx.doi.org/10.1016/j.ejphar.2008.03.028
https://www.ncbi.nlm.nih.gov/pubmed/18466896
https://search.proquest.com/docview/71657935
Volume 587
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