Many previous national and international studies have shown that in patients with PTSD, norepinephrine plays an important role in negative emotions (such as anger and sadness) and arousal symptoms (panic, hyperarousal, flashbacks and intrusive memories), and increases the encoding of conditioned fears and emotional memories. Prenalol has a more promising future as a norepinephrine β-blocker in the prevention and treatment of this disorder. Dr. Hampton reported an experimental study in August 2015 in the Journal of the American Medical Association. The study showed that elevated norepinephrine levels in rats during stress can alter medial prefrontal cortex function, leading to impaired fear elimination and possibly the development of post-traumatic stress disorder. Experiments showed that electric shock stimulation of the rat foot induced a conditioned fear response that altered the firing rate of neurons in the prelimbic (PL) and inferior limbic (IL) areas of the medial prefrontal cortex (mPFC), areas that are implicated in fear expression and elimination. The team also found that propranolol, a norepinephrinergic β-receptor antagonist, restored the balance between PL and IL activity thereby reversing the functional deficit in the mPFC and promoting fear elimination. The investigators hypothesize that the mechanism of action of propranolol in the treatment of PTSD involves the restoration of prefrontal brain function and that patients benefit from the drug rapidly after a traumatic event. There are more drugs currently used in the treatment of PTSD, mainly benzodiazepine anxiolytics, antidepressants, atypical antipsychotics, and anticonvulsants. Low doses of propranolol have also been used successfully in the management of stage fright and behavioral anxiety among others, as it modulates the cognitive representations of body and stress. However, how to better use propranolol in the treatment of PTSD requires a deeper understanding of the drug’s mechanism of action by a wide range of researchers.