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Effects of a short-term exposure to alcohol in rats on FAAH enzyme and CB1 receptor in different brain areas.

Abstract

Acute alcohol exposure in rats (8% ethanol in the liquid diet for a period of 24 h) is associated with a decrease in the levels of endocannabinoids (anandamide and 2-arachidonoyl-glycerol) as well as in various N-acylethanolamines, in different brain regions. In the present study, we wanted to further explore: (i) whether these decreases might be caused by an increase in fatty acid amide hydrolase (FAAH), the enzyme involved in the degradation of N-acylethanolamines including anandamide, and (ii) whether the changes in endocannabinoid levels are accompanied by parallel changes in the major cannabinoid receptor type, the CB(1) receptor, activated by these ligands in the brain. Our data proved that FAAH activity did not increase in any of the four regions analyzed, even it was reduced in the hypothalamus and the prefrontal cortex. Paradoxically, FAAH levels increased in the hypothalamus and, to a lesser extent, in the prefrontal cortex and the amygdala, but not in the caudate-putamen. By contrast, the levels of CB(1) receptors were markedly reduced in the amygdala and prefrontal cortex of these rats, although no changes were seen in the hypothalamus and the caudate-putamen. These results suggest that reductions in the levels of endocannabinoids and related N-acylethanolamines caused by acute alcohol exposure are not originated by an enhanced degradation by FAAH enzyme, but they are associated with low levels of the receptors activated by these ligands, although this parallelism did not occur in all brain regions analyzed. In any case, these observations would support the notion of a general reduction in the activity of the cannabinoid signaling system by acute alcohol exposure.

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  • Authors+Show Affiliations

    ,

    Department of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Faculty of Medicine, Complutense University, 28040 Madrid, Spain.

    , , , ,

    Source

    Drug and alcohol dependence 99:1-3 2009 Jan 01 pg 354-8

    MeSH

    Amidohydrolases
    Animals
    Behavior, Animal
    Blotting, Western
    Body Weight
    Brain Chemistry
    Cannabinoid Receptor Modulators
    Central Nervous System Depressants
    Eating
    Ethanol
    Male
    Rats
    Rats, Sprague-Dawley
    Receptor, Cannabinoid, CB1

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    18922654

    Citation

    Rubio, Marina, et al. "Effects of a Short-term Exposure to Alcohol in Rats On FAAH Enzyme and CB1 Receptor in Different Brain Areas." Drug and Alcohol Dependence, vol. 99, no. 1-3, 2009, pp. 354-8.
    Rubio M, de Miguel R, Fernández-Ruiz J, et al. Effects of a short-term exposure to alcohol in rats on FAAH enzyme and CB1 receptor in different brain areas. Drug Alcohol Depend. 2009;99(1-3):354-8.
    Rubio, M., de Miguel, R., Fernández-Ruiz, J., Gutiérrez-López, D., Carai, M. A., & Ramos, J. A. (2009). Effects of a short-term exposure to alcohol in rats on FAAH enzyme and CB1 receptor in different brain areas. Drug and Alcohol Dependence, 99(1-3), pp. 354-8. doi:10.1016/j.drugalcdep.2008.08.004.
    Rubio M, et al. Effects of a Short-term Exposure to Alcohol in Rats On FAAH Enzyme and CB1 Receptor in Different Brain Areas. Drug Alcohol Depend. 2009 Jan 1;99(1-3):354-8. PubMed PMID: 18922654.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Effects of a short-term exposure to alcohol in rats on FAAH enzyme and CB1 receptor in different brain areas. AU - Rubio,Marina, AU - de Miguel,Rosario, AU - Fernández-Ruiz,Javier, AU - Gutiérrez-López,Dolores, AU - Carai,Mauro A M, AU - Ramos,José A, Y1 - 2008/10/14/ PY - 2008/02/12/received PY - 2008/07/23/revised PY - 2008/08/15/accepted PY - 2008/10/17/pubmed PY - 2009/5/22/medline PY - 2008/10/17/entrez SP - 354 EP - 8 JF - Drug and alcohol dependence JO - Drug Alcohol Depend VL - 99 IS - 1-3 N2 - Acute alcohol exposure in rats (8% ethanol in the liquid diet for a period of 24 h) is associated with a decrease in the levels of endocannabinoids (anandamide and 2-arachidonoyl-glycerol) as well as in various N-acylethanolamines, in different brain regions. In the present study, we wanted to further explore: (i) whether these decreases might be caused by an increase in fatty acid amide hydrolase (FAAH), the enzyme involved in the degradation of N-acylethanolamines including anandamide, and (ii) whether the changes in endocannabinoid levels are accompanied by parallel changes in the major cannabinoid receptor type, the CB(1) receptor, activated by these ligands in the brain. Our data proved that FAAH activity did not increase in any of the four regions analyzed, even it was reduced in the hypothalamus and the prefrontal cortex. Paradoxically, FAAH levels increased in the hypothalamus and, to a lesser extent, in the prefrontal cortex and the amygdala, but not in the caudate-putamen. By contrast, the levels of CB(1) receptors were markedly reduced in the amygdala and prefrontal cortex of these rats, although no changes were seen in the hypothalamus and the caudate-putamen. These results suggest that reductions in the levels of endocannabinoids and related N-acylethanolamines caused by acute alcohol exposure are not originated by an enhanced degradation by FAAH enzyme, but they are associated with low levels of the receptors activated by these ligands, although this parallelism did not occur in all brain regions analyzed. In any case, these observations would support the notion of a general reduction in the activity of the cannabinoid signaling system by acute alcohol exposure. SN - 1879-0046 UR - https://www.unboundmedicine.com/medline/citation/18922654/Effects_of_a_short_term_exposure_to_alcohol_in_rats_on_FAAH_enzyme_and_CB1_receptor_in_different_brain_areas_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0376-8716(08)00319-0 DB - PRIME DP - Unbound Medicine ER -