Individuals with an anxiety disorder commonly struggle with alcohol addiction as well, and researchers have long suggested that the anti-anxiety effects of alcohol motivate some to drink in an effort to self-medicate. However, anxiety is also a symptom of alcohol withdrawal, and some individuals may drink to prevent the onset of withdrawal-related anxiety. A team of researchers from the University of Illinois at Chicago has examined the connection between anxiety and alcohol in rats in the past, and in a recent study, they further studied the biological processes involved. Their results, which appear in the Journal of Neuroscience, indicate a mechanism underlying the trend toward alcoholism in individuals with anxiety.
In a 2006 study, the researchers discovered a connection between alcohol consumption and anxious behavior in rats and brain-derived neurotrophic factor (BDNF), a nerve growth factor that aids in neuron maintenance. In the current study, the researchers continued examining this link by focusing on the way in which BDNF affects production of Arc, a protein found within neurons in the amygdala, which is involved with emotions. Arc changes the shape of neurons, which changes the way the neurons communicate with each other and affects subsequent behavior. Using rats, the researchers observed that brief alcohol consumption increased production of BDNF and Arc, which in turn increased the number of dendritic spines— the branches through which neurons communicate— in neurons in some places within the amygdala. These changes lessened anxious behavior in the rats.
For rats that had consumed alcohol over a longer period of time, however, these anxiety-relieving changes did not occur. When these rats were no longer allowed to drink alcohol, they experienced heightened levels of anxiety accompanied by reduced production of BDNF and Arc and fewer dendritic spines in the amygdala. To reverse the rats' anxiety, the researchers brought their levels of BDNF and Arc back to normal. They then tested this process in control rats by blocking Arc production. Once again, lowered Arc production corresponded with a reduced number of spines in the amygdala and increased anxiety and alcohol consumption. The researchers suggest that while initial alcohol consumption may reduce anxiety, chronic alcohol consumption causes, upon withdrawal, a reduction in BDNF, Arc, and dendritic spines, causing symptoms of anxiety. They suspect that this process contributes to the addictive nature of alcohol, as an individual might continue to drink in order to prevent these symptoms from occurring.
BDNF has been implicated in other psychiatric disorders as well, including schizophrenia, bipolar disorder, and depression, and further research might clarify the role of BDNF and Arc in the development of these conditions. By studying and understanding these biological mechanisms, we may be able to develop new medications that provide effective treatment by targeting these processes. For those struggling with anxiety as well as alcohol addiction, continued research may allow them to better understand and more successfully address both problems.
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