Changes in endocannabinoid contents in the brain of rats chronically exposed to nicotine, ethanol or cocaine

Changes in endocannabinoid contents in the brain of rats chronically exposed to nicotine, ethanol... Despite recent data suggesting that the endocannabinoid transmission is a component of the brain reward system and plays a role in dependence/withdrawal to different habit-forming drugs, only a few studies have examined changes in endocannabinoid ligands and/or receptors in brain regions related to reinforcement processes after a chronic exposure to these drugs. Recently, we carried out a comparative analysis of the changes in cannabinoid CB 1 receptor density in several rat brain regions caused by chronic exposure to some of the most powerful habit-forming drugs. In the present study, we have extended this objective by examining changes in the brain contents of arachidonoylethanolamide (AEA) and 2-arachidonoyl-glycerol (2-AG), the endogenous ligands for cannabinoid receptors, in animals chronically exposed to cocaine, nicotine or ethanol. Results were as follows. Cocaine was the drug exhibiting the minor number of effects, with only a small, but significant, decrease in the content of 2-AG in the limbic forebrain. In contrast, chronic alcohol exposure caused a decrease in the contents of both AEA and 2-AG in the midbrain, while it increased AEA content in the limbic forebrain. This latter effect was also observed after chronic nicotine exposure together with an increase in AEA and 2-AG contents in the brainstem. In contrast, the hippocampus, the striatum and the cerebral cortex exhibited a decrease in AEA and/or 2-AG contents after chronic nicotine exposure. We also tested the effect of chronic nicotine on brain CB 1 receptors, which had not been investigated before, and found an almost complete lack of changes in mRNA levels or binding capacity for these receptors. In summary, our results, in concordance with previous data on CB 1 receptors, indicate that the three drugs tested here produce different changes in endocannabinoid transmission. Only in the case of alcohol and nicotine, we observed a common increase in AEA contents in the limbic forebrain. This observation is important considering that this region is a key area for the reinforcing properties of habit-forming drugs, which might support the involvement of endocannabinoid transmission in some specific events of the reward system activated by these drugs. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Changes in endocannabinoid contents in the brain of rats chronically exposed to nicotine, ethanol or cocaine

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Publisher
Elsevier
Copyright
Copyright © 2002 Elsevier Science B.V.
ISSN
0006-8993
DOI
10.1016/S0006-8993(02)03344-9
Publisher site
See Article on Publisher Site

Abstract

Despite recent data suggesting that the endocannabinoid transmission is a component of the brain reward system and plays a role in dependence/withdrawal to different habit-forming drugs, only a few studies have examined changes in endocannabinoid ligands and/or receptors in brain regions related to reinforcement processes after a chronic exposure to these drugs. Recently, we carried out a comparative analysis of the changes in cannabinoid CB 1 receptor density in several rat brain regions caused by chronic exposure to some of the most powerful habit-forming drugs. In the present study, we have extended this objective by examining changes in the brain contents of arachidonoylethanolamide (AEA) and 2-arachidonoyl-glycerol (2-AG), the endogenous ligands for cannabinoid receptors, in animals chronically exposed to cocaine, nicotine or ethanol. Results were as follows. Cocaine was the drug exhibiting the minor number of effects, with only a small, but significant, decrease in the content of 2-AG in the limbic forebrain. In contrast, chronic alcohol exposure caused a decrease in the contents of both AEA and 2-AG in the midbrain, while it increased AEA content in the limbic forebrain. This latter effect was also observed after chronic nicotine exposure together with an increase in AEA and 2-AG contents in the brainstem. In contrast, the hippocampus, the striatum and the cerebral cortex exhibited a decrease in AEA and/or 2-AG contents after chronic nicotine exposure. We also tested the effect of chronic nicotine on brain CB 1 receptors, which had not been investigated before, and found an almost complete lack of changes in mRNA levels or binding capacity for these receptors. In summary, our results, in concordance with previous data on CB 1 receptors, indicate that the three drugs tested here produce different changes in endocannabinoid transmission. Only in the case of alcohol and nicotine, we observed a common increase in AEA contents in the limbic forebrain. This observation is important considering that this region is a key area for the reinforcing properties of habit-forming drugs, which might support the involvement of endocannabinoid transmission in some specific events of the reward system activated by these drugs.

Journal

Brain ResearchElsevier

Published: Nov 1, 2002

References

  • Chronic ethanol administration down-regulates cannabinoid receptors in mouse brain synaptic plasma membrane
    Basavarajappa, B.S; Cooper, T.B; Hungund, B.L
  • Brain regional distribution of endocannabinoids: implications for their biosynthesis and biological function
    Bisogno, T; Berrendero, F; Ambrosino, G; Cebeira, M; Ramos, J.A; Fernandez-Ruiz, J.J; Di Marzo, V
  • Neuronal nicotinic receptors, important new players in brain function
    Clementi, F; Fornasari, D; Gotti, C
  • Effects of SR141716A on ethanol and sucrose self-administration
    Freedland, C.S; Sharpe, A.L; Samson, H.H; Porrino, L.J
  • Analysis of anandamide, an endogenous cannabinoid substance, and other natural N-acylethanolamines
    Fontana, A; Di Marzo, V; Cadas, H; Piomelli, D
  • Increased motivation for beer in rats following administration of a cannabinoid CB 1 receptor agonist
    Gallate, J.E; Saharov, T; Mallet, P.E; McGregor, I.S
  • Cannabinoid transmission and reward-related events
    Gardner, E.L; Vorel, S.R
  • Lack of morphine-induced dopamine release in the nucleus accumbens of cannabinoid CB 1 receptor knockout mice
    Mascia, M.S; Obinu, M.C; Ledent, C; Parmentier, M; Böhme, G.A; Imperato, A; Fratta, W
  • Anandamide decreases naloxone-precipitated withdrawal signs in mice chronically treated with morphine
    Vela, G; Ruiz-Gayo, M; Fuentes, J.A

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