Document Type

Restricted

Advisor

Joseph Schroeder

Publication Date

2026

Abstract

Individuals with post-traumatic stress disorder (PTSD) commonly report impairments in long-term and working memory, including for emotionally neutral material. Working memory deficits in particular represent one of the most consistently reported cognitive consequences of PTSD and are associated with reduced hippocampal volume and altered prefrontal-hippocampal circuit function. Much of the existing PTSD treatment literature focuses on symptom reduction after the disorder has already developed; comparatively less work has examined pharmacological approaches that may prevent PTSD-related cognitive impairments from emerging following trauma exposure. Propranolol, a β-adrenergic receptor antagonist, has been established as capable of interfering with the consolidation and reconsolidation of fear-related memories, yet its effects on non-aversive cognitive domains such as working memory remain poorly understood. In the present study, we examined whether post-trauma propranolol treatment attenuated stress-induced working memory deficits in a rodent model of social instability stress. Sprague-Dawley rats were assigned to stress-exposed or stress-unexposed conditions and treated with either propranolol or saline following stress exposure; working memory performance was subsequently assessed using the Barnes maze. A significant stress condition × treatment interaction indicated that propranolol-treated stress-exposed animals committed significantly fewer working memory errors than stress-exposed saline controls, with effects most pronounced during the acquisition phase and Trial 1 of each testing day. Propranolol did not impair working memory performance in stress-unexposed animals. These findings suggest that post-trauma β-adrenergic blockade may selectively attenuate stress-induced working memory impairments without producing detrimental effects on non-aversive cognitive function, supporting its potential as a targeted pharmacological intervention for preventing the cognitive consequences of trauma exposure.

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The views expressed in this paper are solely those of the author.