| pubmed-article:6132358 | pubmed:abstractText | One of the many actions of ethanol involves the GABAergic system. The interaction of ethanol with GABAergic neurons is a complex one involving both presynaptic and postsynaptic sites. Through a presumed fluidization of membranes after a single dose of ethanol, the available in vitro evidence suggests that ethanol disrupts the normal functioning of the GABA-benzodiazepine-chloride ionophore complex in a complicated manner involving a sequential activation of different active sites leading to the facilitation of GABA transmission. This finding has been supported in vivo using electrophysiological techniques. Presynaptic GABAergic neurons may experience a reduced activity, especially at low doses of ethanol. After chronic ethanol treatment, GABAergic transmission may be reduced, especially during an ethanol withdrawal syndrome. Also, other changes in the GABA-benzodiazepine-chloride ionophore complex suggest GABA transmission is suppressed postsynaptically. Drugs which enhance the actions of GABA may be suitable inhibitors of the ethanol withdrawal syndrome. In particular a new class of drugs, the triazolopyridazines, may be promising compounds for treatment of withdrawal with a more specific mode of action and fewer side effects. | lld:pubmed |
