The neurotransmitter gamma-aminobutyric acid (GABA) inhibits the activity of signal-receiving neurons by interacting with the GABAA receptor on these cells. The GABAA receptor is a channel-forming protein that allows the passage of chloride ions into the cells. Excessive GABAA activation may play a role in mediating the sedative effects of alcohol and other sedating and anesthetic agents. For example, alcohol enhances the GABAA-mediated chloride flow into cells and may thereby enhance neuronal inhibition. Alcohol’s effects on the GABAA-receptor function likely involve other molecules (e.g., other neurotransmitters and proteins that add phosphate groups to the receptor [i.e., protein kinases]). Several experimental approaches also have suggested that changes in GABAA-receptor function contribute to the tolerance to and dependence on alcohol. Finally, individual differences in the GABA system may play a role in determining a person’s susceptibility to developing alcohol dependence.