Introduction: Post-traumatic stress disorder (PTSD) is the most prevalent neuropsychiatric disorder developed by vulnerable individuals exposed to life-threatening events. Fear extinction deficits results from decreased medial prefrontal (mPFC) activity and are a key feature of PTSD. Also, it has been shown that brain dopamine receptors are involved in fear extinction that drives learning and memory. Furthermore, dopaminergic (DAergic) dysfunction is implicated in the pathophysiology of PTSD and, as a consequence, drugs targeting the central DAergic system could have a therapeutic value for the management of this disorder. Methodsand Materials: We conducted a thorough and methodical search for pertinent references using different databases, including Pubmed, Embase, MEDLINE, Scopus, Web of Science Core Collection, and Google Scholar by using combinations of keywords such as "PTSD," " dopaminergic System," "Extinction," "Facilitation," "Therapeutic methods," "Pharmacological,”. The keywords were searched in the "title/abstract" field of these databases. The resulting articles were then carefully selected for their relevance to the topic at hand. Results:Findings revealed that individuals with PTSD display fear extinction deficits raises the possibility that corticolimbic circuitry and related dopaminergic system may mediate fear memory extinction via underlying mechanisms. Also,dopaminergic mechanisms relevant for the pathogenesis of PTSD, as well as potential dopaminergic-based pharmacotherapies are discussed in the context of addressing the unmet medical need for new and effective drugs for the treatment of PTSD. Conclusion: Due to dopaminergic mechanisms' involvement in fear extinction, potential dopaminergic-based pharmacotherapies could be a promising strategy in PTSD treatment via addressing the unmet medical need for new and effective drugs for the treatment of PTSD.