Mechanisms that may underlie the behavioural effects of ethanol

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      Twenty percent enhancement of GABA-induced chloride currents is achieved at 30 mM EtOH (Nishio and Narahashi, 1990), 40% enhancement of serotonin-induced current occurs at 50 mM EtOH (Lovinger, 1991), and the EC50 for functional blockade of α4β2-nicotinic acetylcholine receptors (nAChRs) is 75 mM (Zuo et al., 2002). In human drinkers, however, blood alcohol levels are 6–13 mM (<15 mM) for some impairment of attention but not legal intoxication, 17 mM (0.08%) for most legal definitions of inebriation (triple risk for an accident; impaired reasoning, perception and reaction time), 20–22 mM for sedation and ataxia, 50 mM for loss of consciousness, and 110 mM or higher for death (Little, 1991). Therefore, there remains a gap in our understanding of mechanisms and molecular targets involved at lower doses (<10 mM) of EtOH that are relevant to reward and dependence and for the treatment of AUD.

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      Acute ethanol administration has been reported to alter the excitability of neurons and to modulate synaptic transmission. In central neurons, ethanol has been shown to act on various membrane receptors, such as the NMDA or GABAA-receptors, as well as on voltage-gated ion channels, especially Ca2+ channels (Little, 1991; Weight, 1992). Ethanol has diverse effects on the expression of various mRNAs within the CNS, including ion channels, neuropeptides, membrane receptors and many immediate early genes (Crews et al., 1996).

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