Ethanol, GABA and epilepsy

Ethanol exerts its behavioral effects largely by interacting with receptors to brain neurotransmitters, The molecular mechanisms involving these inter actions are still not well known since an ideal model for their study is cu rrently unavailable. In addition, responses to alcohol may vary due to fact ors such as genetic predisposition, ethanol concentration consumed, and sti muli such as stress, socialization, etc. The chronic consumption of alcohol, similar to that of other drugs such as benzodiazepines and barbiturates, is linked to GABAergic neurotransmission. GABA is the predominant inhibitory neurotransmitter in the brain. In a con text of substance abuse, these three drugs first cause a gratifying effect, later tolerance and finally, physical and psychological dependence. If con sumption is interrupted abruptly, a withdrawal syndrome occurs. The Alcohol Withdrawal Syndrome (AWS) is a state of hyperexcitability characterized by anxiety, fear, muscular rigidity and tonic-clonic seizures with epileptifo rm-type characteristics. The epileptic seizures seen during AWS are often s imilar to those seen in experimental epilepsy models such as "kindling" or GABA Withdrawal Syndrome (GWS) models. A possible correlation between these models and AWS will allow for a better understanding of the cellular and m olecular effects that alcohol exerts on the brain. (C) 1999 IMSS. Published by Elsevier Science Inc.