Stress and PTSD Mechanisms as Targets for Pharmacotherapy of Alcohol Abuse, Addiction, and Relapse
Annual rept. 30 Sep 2014-29 Sep 2015
SEATTLE INST FOR BIOMEDICAL AND CLINICAL RESEARCH SEATTLE WA
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We have demonstrated that alcohol-naive rats exhibiting high acoustic startle response which is associated with increased anxiety-like behavior develop increased subsequent alcohol intake and alcohol preference in an intermittent alcohol access IAA paradigm. The development of increased alcohol intake and increased alcohol preference was highly correlated with acoustic startle amplitude previously determined before the initial access to alcohol. This study, which is key to this entire project, has been published. A new key accomplishment is our recent demonstration that suppression of noradrenergic signaling at the time of traumatic stress decreases acquisition of increased voluntary alcohol drinking long after the stress, which provides a new model for preventive treatment. The schedule for this study was advanced to year 2 instead of the orginally proposed year 3 due to the urgent need for new theerapies to prevent PTSD and alcohol abuse in response to trauma. Preliminary results were recently presented at the 2015 Internatiional Society for PsychoNeuroEndocrinology meeting, and the study will be published after analyses of final data. It has again been necessary to replace a research scientist, causing delays, but all remaining studies and analyses using rat models to address stress and PTSD mechanisms as targets for pharmacotherapy of PTSD and associated alcohol abuse are progressing toward completion as planned.