![\"](\"https:\/\/www.med.unc.edu\/alcohol\/wp-content\/uploads\/sites\/515\/2017\/12\/Kashweb.jpg\" "\\"Kash")
One of the most troubling, and difficult to treat, aspects of alcoholism, is relapse. Relapse occurs when an individual who has stopped consuming alcohol begins drinking again. There are numerous reasons for relapse to occur, yet one of the most commonly cited causes is stress. It has been hypothesized that chronic exposure to alcohol leads to the emergence of a negative emotional state. This negative emotional state is thought to contribute to relapse behavior, as individuals ingest alcohol as a means of relief. This altered behavior is believed to be caused by persistent adaptations in discrete brain regions that underlie stress responsivity. One brain structure that is thought to be a site of important adaptations underlying this behavior is the Bed Nucleus of the Stria Terminalis (BNST). This structure is a critical regulator of behavioral and physiological activation associated with anxiety. Recent reports suggest that activation of serotonin receptors in the BNST can govern emotional state, specifically anxiety. Our preliminary data indicate that serotonin signaling is altered in the BNST following a chronic exposure to alcohol. The experiments in this ABMRF proposal will utlilize molecular and electrophysiological approaches to identify specific alterations in serotonin signaling in the BNST that may contribute to increased anxiety-like behavior following chronic ethanol exposure. Given the critical role that these long lasting behavioral deficits are believed to play in alcohol abuse and relapse, understanding molecular mechanisms that underlie this process could lead to more effective therapeutic interventions.<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"