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JAMA
Tracy Hampton, PhD
Previous studies have indicated that norepinephrine signaling—which plays an important role in mood and arousal as well as in the encoding, retrieval, and reconsolidation of emotional memories—is elevated in individuals with posttraumatic stress disorder (PTSD), and drugs that block norepinephrine receptors may be promising in preventing and treating PTSD.
New research in rats reveals that norepinephrine signaling in response to stress can alter the function of the medial prefrontal cortex, leading to impaired fear extinction and possibly PTSD (Fitzgerald PJ et al. Proc Natl Acad Sci U S A. doi:10.1073/pnas.1500682112 [published online June 29, 2015]). Investigators at Texas A&M University, in College Station, found that foot-shock stress accompanied by fear conditioning changed both the firing rate and bursting characteristics of neurons in the prelimbic (PL) and infralimbic (IL) regions of the medial prefrontal cortex (mPFC) implicated in fear expression and fear extinction, respectively.
The team also discovered that the β-noradrenergic receptor antagonist propranolol can reverse functional deficits in the mPFC by restoring the balance between PL and IL activity and thereby facilitate fear extinction that is otherwise disrupted by stress. The findings suggest that the possible mechanism of propranolol in the treatment of PTSD may involve normalizing prefrontal cortical function and may be most beneficial soon after the traumatic event, when stress is high.