Heavy alcohol drinking is a widespread and costly problem that affects millions of people worldwide. It can lead to various health and social issues, such as liver disease, cancer, violence, and accidents. However, the underlying mechanisms of alcohol addiction are not fully understood, and the available treatments are limited and often ineffective. A new study by researchers at Boston University has identified a key mediator in the brain that contributes to heavy alcohol drinking and could be a potential target for new therapies.
The study, published in the journal ScienceDaily, focused on a peptide called pituitary adenylate cyclase-activating polypeptide (PACAP), which is involved in stress and pain responses. The researchers found that PACAP levels were increased in the brain area called the bed nucleus of the stria terminalis (BNST) in an experimental model of heavy, intermittent alcohol drinking. The BNST is known to be involved in the behavioral response to stress and in chronic alcohol use.
The researchers then used a virus to block the neural pathways containing PACAP that specifically arrive to the BNST. They found that this intervention dramatically reduced heavy alcohol drinking in the experimental model, suggesting that PACAP mediates the addictive properties of alcohol.
The study also found that another peptide related to PACAP, called calcitonin gene-related peptide (CGRP), was also increased in the BNST during alcohol withdrawal. Both peptides have been implicated in stress and pain sensitivity, but their role in alcohol addiction is less established.
The researchers concluded that their findings provide evidence for a key role of PACAP in heavy alcohol drinking and offer new avenues for developing novel pharmacological therapies for alcohol use disorder.