The cannabinoid antagonist AM251 attenuates nicotine self-administration and nicotine-seeking behaviour in rats

The cannabinoid antagonist AM251 attenuates nicotine self-administration and nicotine-seeking... The cannabinoid receptor subtype (CB 1 ) antagonist rimonabant (SR141716) has been shown to decrease nicotine self-administration and attenuate nicotine-evoked dopamine release in the nucleus accumbens; effects that support recent findings on its clinical efficacy as a smoking cessation aid. The present experiments aim to advance our understanding on the role of CB 1 receptors in rodent models of nicotine dependence. AM251, a selective antagonist at CB 1 receptors dose-dependently (1, 3 and 10 mg/kg IP) suppressed intravenous nicotine (0.03 mg/kg per infusion) self-administration in rats during three successive days of pre-treatment. This reduction was short lasting since behaviour was reinstated by suspending AM251 pre-treatment. This was relatively specific to nicotine self-administration since the profile of these reductions produced by AM251 was significantly different from the responses maintained by food pellets. In a model of nicotine-seeking behaviour, rats that had been extinguished by removal of nicotine and associated cues, and presented with a priming dose of nicotine (0.2 mg/kg SC) with the cues, showed robustly reinstated responses to nicotine-seeking behaviour. Acute pre-treatment with AM251 (1–10 mg/kg IP) dose-dependently attenuated the reinstatement effects produced by nicotine and the contingently presented cues. These preclinical findings support the use of rimonabant as a smoking cessation aid and highlight the CB 1 receptor as a viable target to control intake of nicotine and prevent relapse. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuropharmacology Elsevier

The cannabinoid antagonist AM251 attenuates nicotine self-administration and nicotine-seeking behaviour in rats

Neuropharmacology, Volume 54 (2) – Feb 1, 2008

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Publisher
Elsevier
Copyright
Copyright © 2007 Elsevier Ltd
ISSN
0028-3908
eISSN
1873-7064
D.O.I.
10.1016/j.neuropharm.2007.10.011
Publisher site
See Article on Publisher Site

Abstract

The cannabinoid receptor subtype (CB 1 ) antagonist rimonabant (SR141716) has been shown to decrease nicotine self-administration and attenuate nicotine-evoked dopamine release in the nucleus accumbens; effects that support recent findings on its clinical efficacy as a smoking cessation aid. The present experiments aim to advance our understanding on the role of CB 1 receptors in rodent models of nicotine dependence. AM251, a selective antagonist at CB 1 receptors dose-dependently (1, 3 and 10 mg/kg IP) suppressed intravenous nicotine (0.03 mg/kg per infusion) self-administration in rats during three successive days of pre-treatment. This reduction was short lasting since behaviour was reinstated by suspending AM251 pre-treatment. This was relatively specific to nicotine self-administration since the profile of these reductions produced by AM251 was significantly different from the responses maintained by food pellets. In a model of nicotine-seeking behaviour, rats that had been extinguished by removal of nicotine and associated cues, and presented with a priming dose of nicotine (0.2 mg/kg SC) with the cues, showed robustly reinstated responses to nicotine-seeking behaviour. Acute pre-treatment with AM251 (1–10 mg/kg IP) dose-dependently attenuated the reinstatement effects produced by nicotine and the contingently presented cues. These preclinical findings support the use of rimonabant as a smoking cessation aid and highlight the CB 1 receptor as a viable target to control intake of nicotine and prevent relapse.

Journal

NeuropharmacologyElsevier

Published: Feb 1, 2008

References

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