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Changes in endocannabinoid content in the brain of rats chronically exposed to nicotine, ethanol or cocaine (Articolo in rivista)
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- Changes in endocannabinoid content in the brain of rats chronically exposed to nicotine, ethanol or cocaine (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
Gonzalez S., Cascio M.G., Fernandez-Ruiz J., Fezza F., Di Marzo V., Ramos J.A. (2002)
Changes in endocannabinoid content in the brain of rats chronically exposed to nicotine, ethanol or cocaine
in Brain research
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- Gonzalez S., Cascio M.G., Fernandez-Ruiz J., Fezza F., Di Marzo V., Ramos J.A. (literal)
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- ISI Web of Science (WOS) (literal)
- Titolo
- Changes in endocannabinoid content in the brain of rats chronically exposed to nicotine, ethanol or cocaine (literal)
- 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.
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