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Proteins --- Proteins. --- Gene Products, Protein --- Gene Proteins --- Protein Gene Products --- Proteins, Gene --- Molecular Mechanisms of Pharmacological Action --- Periodicals --- Protein

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Background: Ethanol exerts its action on neurons through several mechanisms. Because of its small size, ethanol is not a very specific ligand. This characteristic may explain the low specificity of the effects of ethanol.
Methods: Given the extent of my thesis subject, my review was limited to articles published between 2000 and 2009. this examination is based on the contents of synthesis articles published in 2008.
Results: Ethanol alters the fluidity of neuronal membranes. This effect is offset by the homeostatic mechanisms that restore the initial rigidity. Upon the discontinuation of a chronic consumption of ethanol, a rigidity excess of neuronal membranes can be observed. Ethanol also modifies the activity if neurotransmitters, neurotrophins and neurosteroids. These effects may be the cause f acute exposure, chronic exposure of withdrawal.
Conclusions : Ethanol acts primarily by modifying synaptic transmission within the central nervous system. This change involves in particular several neurotransmitters: glutamate, GABA, dopamine, adenosine, serotonin, endogenous opioids, neuropeptides and endocannabinoids. Many of these neurotransmitters are considered as potential targets for the pharmacological treatment of alcoholism Contexte: L’éthanol exerce son action sur les neurones par l’intermédiaire de nombreux mécanismes. Du fait de sa petite taille, l’éthanol ne constitue pas un ligand très spécifique. Cette caractéristique peut expliquer la faible spécificité des effets de l’éthanol.
Méthodes : Au regard de l’étendue de mon sujet de mémoire, je me suis limitée à la recherche d’articles publiés entre 2000 et 2009. Cette recherche a été basée sur le contenu d’articles de synthèse publiés en 2008.
Résultats : L’éthanol modifie la fluidité des membranes neuronales. Cet effet est compensé par les mécanismes homéostatiques qui rétablissent la rigidité initiale. Lors de l’arrêt d’une consommation chronique d’éthanol, on observe un excès de rigidité des membranes neuronales. L’éthanol modifie également l’activité des neurotransmetteurs, des neurotrophines et des neurostéroïdes. Ces effets peuvent être la cause d’une exposition aiguë, d’une exposition chronique ou d’un sevrage.
Conclusions :L’éthanol agit principalement en modifiant la transmission synaptique au niveau du système nerveux central. Cette modification implique particulièrement plusieurs neurotransmetteurs : le glutamate, le GABA, la dopamine, l’adénosine, la sérotonine, les opioïdes endogènes, les neuropeptides et les endocannabinoïdes. La plupart de ces neurotransmetteurs sont considérés comme étant des cibles potentielles pour le traitement pharmacologique de l’alcoolisme

Ethanol --- Ethanol --- Neurotransmitter Agents --- Nerve Growth Factors --- Substance-Related Disorders --- Molecular Mechanisms of Pharmacological Action --- Central Nervous System Agents

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Proteins --- Proteins. --- Gene Products, Protein --- Gene Proteins --- Protein Gene Products --- Proteins, Gene --- Proteids --- Molecular Mechanisms of Pharmacological Action --- Biomolecules --- Polypeptides --- Proteomics --- Protein

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Proteins --- Proteins. --- Protéines --- Proteids --- Gene Products, Protein --- Gene Proteins --- Protein Gene Products --- Proteins, Gene --- Molecular Mechanisms of Pharmacological Action --- Biomolecules --- Polypeptides --- Proteomics --- Protéines --- Protein --- Protéines. --- protein.

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Enzymes. --- Biocatalysts --- Molecular Mechanisms of Pharmacological Action --- Clinical enzymology. --- Enzymes --- Laboratory manuals. --- Clinical enzymology --- Ferments --- Soluble ferments --- Catalysts --- Proteins --- Enzymology --- Diagnostic enzymology --- Clinical chemistry --- Biocatalyst --- Enzyme