Neuropharmacological and clinical aspects of alcohol withdrawal.
Abnormalities in the function or activity of several neurotransmitter systems have been demonstrated after acute and chronic, exposure to alcohol, and in alcohol withdrawal. The changes can be divided into alterations in function of inhibitory and excitatory systems. Inhibitory dysfunction is indicated by reduced gamma-aminobutyric acid and alpha-2-adrenoceptor activity. In conjunction with, and exacerbating this, is increased activity of excitatory systems, perhaps the most significant of which is the probable potentiation of N-methyl-D-aspartate activity by depletion of magnesium. There is additional, and possibly secondary, overactivity of catecholamine and corticotropin releasing factor neuronal systems. Other, less specific changes include increased numbers of calcium channels, which would increase neuronal excitability. The evidence for these changes is presented, and the implications for new treatment regimes for alcohol withdrawal are discussed.
Nutt
D J
DJ
Reckitt and Colman Psychophamacology Unit, School of Medical Sciences, Bristol, U.K.
Glue
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P
D000435:Alcoholic Intoxication / Q000378:metabolism*; D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D006801:Humans; D009474:Neurons / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism* / Q000502:physiology; D013375:Substance Withdrawal Syndrome / Q000378:metabolism*
D018377:Neurotransmitter Agents