Neuroscientists at the Scripps Research Institute have made a significant discovery that may have implications for individuals suffering from post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) simultaneously. Their research, published in Molecular Psychiatry, demonstrates that inhibiting neurons involved in the body's stress response can potentially decrease alcohol consumption in individuals with comorbid PTSD and AUD, even if they continue to experience trauma-related anxiety.

The study, led by senior author Marisa Roberto, PhD, examined the role of corticotropin-releasing factor (CRF) producing neurons in the central amygdala in regulating alcohol use in response to stress. The researchers used a rat model to show that reducing the activity of these neurons resulted in decreased alcohol intake without affecting anxiety levels related to trauma.

The comorbidity of PTSD and AUD highlights the need to understand and treat these conditions together. Approximately 6% of the U.S. population will develop PTSD at some point, and individuals with PTSD have a 30% lifetime prevalence of AUD. However, there are currently limited pharmaceutical therapies available for treating these disorders simultaneously.

In previous studies, Roberto's team had developed a rat model that exhibited symptoms similar to comorbid PTSD and AUD in humans, including aggression, anxiety, hyperarousal, disturbed sleep, and increased alcohol consumption. In this new study, the researchers compared stressed rats with those that did not exhibit anxiety-like behaviors by providing both groups access to alcohol and water.

The stressed rats showed higher levels of peripheral stress hormones, as well as altered gene expression in the central amygdala, including increased levels of CRF. CRF plays a crucial role in regulating physiological responses to stress and has been linked to excessive drinking. Prior research showed that inhibiting neurons that express CRF can reduce alcohol consumption.

To test their hypothesis, the researchers inhibited CRF-producing neurons in the stressed rats. They discovered that this intervention indeed led to decreased alcohol consumption. However, contrary to their expectations, it did not alleviate anxiety as they had initially anticipated.

Lead author Bryan Cruz, PhD, highlighted that other neuropeptides may be involved in trauma-induced anxiety alongside CRF. Further research is necessary to unravel the intricate neurobiology of stress-related alcohol consumption and trauma-induced anxiety in individuals with comorbid PTSD and AUD.

These findings shed light on the complex relationship between stress, trauma, and alcohol use while opening up new avenues for potential therapeutic interventions targeting specific neural pathways associated with stress-induced drinking behaviors. The research conducted at Scripps Research Institute contributes to a better understanding of the underlying neurological mechanisms of comorbid PTSD and AUD, ultimately aiding in the development of future intervention strategies for these debilitating disorders.

The study was supported by funding from the National Institute on Alcohol Abuse and Alcoholism, as well as the Schimmel Family Chair and Pearson Center for Alcoholism and Addiction Research. The team of authors included researchers from Scripps Research, The University of Tennessee Health Science Center, and The University of Texas at Austin.

Overall, this research brings hope for individuals dealing with the challenging comorbidity of PTSD and AUD, offering potential new treatment options to improve their quality of life.