Scientists have identified a brain mechanism in rats that may play a central role in regulating anxiety
and alcohol consumption. The finding by researchers supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH), could provide important clues about the neurobiology of drinking behaviors in humans. A report of the study appears in the October 3, 2005, issue of The Journal of Clinical Investigation
Researchers found that "P" rats, a strain bred to prefer alcohol, showed more anxiety-like behaviors and drank more alcohol than non alcohol-preferring "NP" rats.
Researchers also found that levels of CREB, a protein involved in a variety of brain functions, were lower in certain brain areas of P rats compared with NP rats. Levels of neuropeptide Y (NPY), a molecule that regulates the function of several neurotransmitters and that is known to play a role in anxiety and drinking behaviors, were also lower in P rats. One function of CREB is to regulate the production of NPY.
Alcohol intake reduced anxiety-like behaviors in the P rats, an effect that was associated with increased CREB function and NPY production in the central and medial amygdala (a part of the brain). Furthermore, by administering compounds that promote CREB function and NPY production in the central amygdala, researchers were able to reduce anxiety -- and alcohol intake -- in P rats.
On the other hand, by disrupting CREB function (and the accompanying NPY production) in the central amygdala of NP rats, the researchers were able to provoke anxiety-like behavior and promote alcohol intake in those animals.
Researchers proposed that decreased CREB-dependent NPY production in the central amygdala might be a pre-existing condition for anxiety and drinking behaviors.
Their finding suggested a genetic predisposition to high anxiety and drinking behaviors of P rats. Future studies will likely explore the relationship of other CREB-related compounds to these phenomena in P rats or other animal models.