Mechanisms of alcohol withdrawal syndrome.
The basic mechanism or mechanisms of the alcohol withdrawal syndrome (AWS) are still unknown despite extensive research on alcoholism. There are, however, two major hypotheses or groups of hypotheses. Increasing experimental evidence supports adaptive changes in membrane lipids and/or proteins in response to prolonged high alcohol concentrations which might cause abnormal function after withdrawal of alcohol in general or more specifically in certain receptor sites. Changes in the formation or concentration of some receptor ligands as a consequence of alcohol metabolism are, however, also possible. Both can cause changes in neurotransmission, and these have been found in several systems. Although all studies do not agree, there seems to be some reduction in gabaergic, enkephalinergic, and possibly in dopaminergic function and increase in glutaminergic, adrenergic, cholinergic and possibly in serotoninergic and tryptaminergic activity at least in some neurons during AWS. These may be involved in producing some symptoms, but the variable whole AWS, particularly its two phases, remains to be explained.
D000431:Ethanol / Q000009:adverse effects* / Q000378:metabolism; D006801:Humans; D018377:Neurotransmitter Agents / Q000502:physiology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D009435:Synaptic Transmission
D018377:Neurotransmitter Agents; D000431:Ethanol