Neuropathology of comorbid anxiety disorders and alcohol dependence

consumption for NP or P rats after shock. This lack of significance was not consistent with our hypothesis. Possible explanations are: • Possible delay in post shock consumption • Shock strength not strong enough to elicit stress-induced alcohol consumption in home cage. • Extinction & Post Extinction: Alcohol consumption in NP and P rats did not impair consolidation of fear memory, nor fear expression during the extinction test. However, alcohol impaired acquisition of fear extinction only in P rats. Because P rats had lower freezing overall, they were either impaired in encoding of the fear event, or switched to escape behaviors. Ongoing analyses will dissociate between the two. • EPM: After the first extinction session, P rats spent less time in the open arms in the EPM than control NP rats. Interestingly, shock P rats behaved similarly to shock + EtOH or control P rats. This is consistent with the hypothesis that P rat behaved in a more ‘impulsive’ manner and possibly showed maladaptive responses to shock. This change in behavior was reversed by alcohol. • Analysis is ongoing, however, current data suggests that alcohol may lead to an impairment of fear extinction in P rats, but not NP rats. Consistent with that, alcohol also impairs IEG expression in the prefrontal cortex only in P rats. Further investigations, including outbred rats, will shed more light on how alcohol is affecting memory formation in P and NP rats. INTRODUCTION