Early life stress (ELS) produces an increased vulnerability for post-traumatic stress disorder (PTSD). One of the hallmark characteristics of PTSD is an increase in fear responding over time (Elharrar et al., 2013). Using a well-established rodent model developed in our lab between early life adversity and the development of PTSD-like phenotype, which we call stress-enhanced fear learning (SEFL) (Quinn et al., 2014), we examined the effects of propranolol (PR), a β-Adrenergic antagonist, on both stress sensitization and memory consolidation. This study used 32 mice which were either exposed or not exposed to ELS. Following the stress experience, the mice were injected with either propranolol (10 mg/kg/10mL ) or vehicle. In Context A, the mice who did not experience ELS were expected to show no significant freezing and mice who received 15 footshocks and vehicle were expected to show robust freezing compared to the PR mice which were expected to show a freezing deficit. In Context B, the mice who did not experience ELS were expected to show moderate levels of freezing while mice who experienced 15 footshocks were expected to show stress-enhanced fear learning (greater freezing) regardless of drug injection. If results were as expected, the presence of SEFL with the post-fear conditioning administration of PR would suggest that the mechanisms underlying SEFL must deal with the stress experience and not stress sensitization. This would agree with our current understanding of PR and its diminutive effect on the associative memory of stressful events, but not on future threats. Future studies should focus on the administration of PR prior to the ELS session in order to assess whether PR affects both stress sensitization effects and memory consolidation with the hope of one day using PR as an effective treatment for PTSD.
Author: Manuel Acuna, Elle Henley, Kate Brand
Faculty Advisor: Jennifer Quinn, Psychology
Graduate Student Advisor: Amanda Reichert, Psychology
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