The neurotransmitter gamma-aminobutyric acid (GABA) inhibits the activ
ity 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 ac
tivation may play a role in mediating the sedative effects of alcohol
and other sedating and anesthetic agents. For example, alcohol enhance
s 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 prote
ins that add phosphate groups to the receptor [i.e., protein kinases])
. Several experimental approaches also have suggested that changes in
GABA(A)-receptor function contribute to the tolerance to and dependenc
e on alcohol. Finally, individual differences in the GABA system may p
lay a role in determining a person's susceptibility to developing alco
hol dependence.