Bases bioquímicas y neurobiológicas de la adicción al alcohol

Abstract

Recent advances in neuroscience have made it possible to deepen into the physiopathology of alcoholism at a biochemical and cellular level. There is now good evidence that acute effects of alcohol are mediated through interactions with amino acid neurotransmitters (mainly at GABAA and NMDA receptors) plus parallel changes in amines such as dopamine and noradrenaline. Neuroadaptative responses at amino acid receptors probably underlie significant components of the withdrawal syndrome and contribute to neuronal death found in chronic alcoholism. Although not so well understood, ethanol reinforcing properties appear to be mainly mediated by activation of GABAA receptors, release of opioid peptides, interaction with nicotinic receptors and indirect release of dopamine.