The researchers found that a particular protein in the amygdala controlled the drinking behavior of laboratory animals. Rats that were chronically fed alcohol showed high levels of anxiety when alcohol was withdrawn from their diet. In the early phases of withdrawal, levels of the active form of a protein abbreviated as CREB were low in certain areas of the amygdala.

However, when alcohol was present in the bloodstream or when normal levels of active protein were restored experimentally, the anxiety behaviors in the alcohol-dependent animals vanished.

"Some 30 to 70 percent of alcoholics are reported to suffer from anxiety, and depression -- drinking is a way for these individuals to self-medicate," said Subhash Pandey, lead author. "If we can control the psychological symptoms, perhaps we can help many of the millions of Americans who are victims of alcohol addiction."

When the CREB protein, formally called cyclic AMP responsive element binding protein, is activated, it regulates the manufacture of neuropeptide Y. In the laboratory studies, low levels of active protein or of neuropeptide Y correlated with symptoms of anxiety and excessive alcohol consumption.

In normal rats, the researchers blocked production of neuropeptide Y. With lower levels of neuropeptide Y, the animals showed signs of anxiety and their alcohol consumption increased. When levels of neuropeptide Y were restored by infusing it into the central amygdala, the rats' excessive drinking behavior ceased.