Regulation of brain anandamide by acute administration of ethanol

Belen Ferrer, Francisco Javier Bermúdez-Silva, Ainhoa Bilbao, Lily Alvarez-Jaimes, Irene Sanchez-Vera, Andrea Giuffrida, Antonia Serrano, Elena Baixeras, Satishe Khaturia, Miguel Navarro, Loren H. Parsons, Daniele Piomelli, Fernando Rodríguez De Fonseca

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45-90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

Original languageEnglish (US)
Pages (from-to)97-104
Number of pages8
JournalBiochemical Journal
Volume404
Issue number1
DOIs
StatePublished - May 15 2007

Fingerprint

Brain
Ethanol
Nucleus Accumbens
4 alpha-glucanotransferase
Fatty Acids
Amidohydrolases
Tissue
Acyltransferases
Degradation
Phospholipase D
Cannabinoids
Enzymes
anandamide
Cerebellum
Adipose Tissue
Glutamic Acid
Hippocampus
Phospholipids
Membranes
Plasmas

Keywords

  • Alcohol
  • Anandamide
  • Arachidonoylethanolamide (AEA)
  • Cannabinoid
  • Fatty acid amidohydrolase (FAAH)
  • Hippocampus

ASJC Scopus subject areas

  • Biochemistry

Cite this

Ferrer, B., Bermúdez-Silva, F. J., Bilbao, A., Alvarez-Jaimes, L., Sanchez-Vera, I., Giuffrida, A., ... Rodríguez De Fonseca, F. (2007). Regulation of brain anandamide by acute administration of ethanol. Biochemical Journal, 404(1), 97-104. https://doi.org/10.1042/BJ20061898

Regulation of brain anandamide by acute administration of ethanol. / Ferrer, Belen; Bermúdez-Silva, Francisco Javier; Bilbao, Ainhoa; Alvarez-Jaimes, Lily; Sanchez-Vera, Irene; Giuffrida, Andrea; Serrano, Antonia; Baixeras, Elena; Khaturia, Satishe; Navarro, Miguel; Parsons, Loren H.; Piomelli, Daniele; Rodríguez De Fonseca, Fernando.

In: Biochemical Journal, Vol. 404, No. 1, 15.05.2007, p. 97-104.

Research output: Contribution to journalArticle

Ferrer, B, Bermúdez-Silva, FJ, Bilbao, A, Alvarez-Jaimes, L, Sanchez-Vera, I, Giuffrida, A, Serrano, A, Baixeras, E, Khaturia, S, Navarro, M, Parsons, LH, Piomelli, D & Rodríguez De Fonseca, F 2007, 'Regulation of brain anandamide by acute administration of ethanol', Biochemical Journal, vol. 404, no. 1, pp. 97-104. https://doi.org/10.1042/BJ20061898
Ferrer B, Bermúdez-Silva FJ, Bilbao A, Alvarez-Jaimes L, Sanchez-Vera I, Giuffrida A et al. Regulation of brain anandamide by acute administration of ethanol. Biochemical Journal. 2007 May 15;404(1):97-104. https://doi.org/10.1042/BJ20061898
Ferrer, Belen ; Bermúdez-Silva, Francisco Javier ; Bilbao, Ainhoa ; Alvarez-Jaimes, Lily ; Sanchez-Vera, Irene ; Giuffrida, Andrea ; Serrano, Antonia ; Baixeras, Elena ; Khaturia, Satishe ; Navarro, Miguel ; Parsons, Loren H. ; Piomelli, Daniele ; Rodríguez De Fonseca, Fernando. / Regulation of brain anandamide by acute administration of ethanol. In: Biochemical Journal. 2007 ; Vol. 404, No. 1. pp. 97-104.
@article{daaeb00f66d94045983c4b93b47d8760,
title = "Regulation of brain anandamide by acute administration of ethanol",
abstract = "The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45-90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.",
keywords = "Alcohol, Anandamide, Arachidonoylethanolamide (AEA), Cannabinoid, Fatty acid amidohydrolase (FAAH), Hippocampus",
author = "Belen Ferrer and Berm{\'u}dez-Silva, {Francisco Javier} and Ainhoa Bilbao and Lily Alvarez-Jaimes and Irene Sanchez-Vera and Andrea Giuffrida and Antonia Serrano and Elena Baixeras and Satishe Khaturia and Miguel Navarro and Parsons, {Loren H.} and Daniele Piomelli and {Rodr{\'i}guez De Fonseca}, Fernando",
year = "2007",
month = "5",
day = "15",
doi = "10.1042/BJ20061898",
language = "English (US)",
volume = "404",
pages = "97--104",
journal = "Biochemical Journal",
issn = "0264-6021",
publisher = "Portland Press Ltd.",
number = "1",

}

TY - JOUR

T1 - Regulation of brain anandamide by acute administration of ethanol

AU - Ferrer, Belen

AU - Bermúdez-Silva, Francisco Javier

AU - Bilbao, Ainhoa

AU - Alvarez-Jaimes, Lily

AU - Sanchez-Vera, Irene

AU - Giuffrida, Andrea

AU - Serrano, Antonia

AU - Baixeras, Elena

AU - Khaturia, Satishe

AU - Navarro, Miguel

AU - Parsons, Loren H.

AU - Piomelli, Daniele

AU - Rodríguez De Fonseca, Fernando

PY - 2007/5/15

Y1 - 2007/5/15

N2 - The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45-90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

AB - The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45-90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

KW - Alcohol

KW - Anandamide

KW - Arachidonoylethanolamide (AEA)

KW - Cannabinoid

KW - Fatty acid amidohydrolase (FAAH)

KW - Hippocampus

UR - http://www.scopus.com/inward/record.url?scp=34248998840&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34248998840&partnerID=8YFLogxK

U2 - 10.1042/BJ20061898

DO - 10.1042/BJ20061898

M3 - Article

C2 - 17302558

AN - SCOPUS:34248998840

VL - 404

SP - 97

EP - 104

JO - Biochemical Journal

JF - Biochemical Journal

SN - 0264-6021

IS - 1

ER -