期刊
CNS DRUGS
卷 27, 期 3, 页码 221-232出版社
ADIS INT LTD
DOI: 10.1007/s40263-013-0051-4
关键词
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资金
- National Institutes of Health [R21 MH081103, R21 MH096105-01A1, R21 MH085627, R01 MH096876-01A1]
- NATIONAL INSTITUTE OF MENTAL HEALTH [R21MH081103, R21MH085627, R01MH096876, R21MH096105] Funding Source: NIH RePORTER
Post-traumatic stress disorder (PTSD) is a common and chronic anxiety disorder that can result after exposure to a traumatic event. Though our understanding of the aetiology of PTSD is incomplete, several neurobiological systems have been implicated in the pathophysiology and vulnerability towards developing PTSD after trauma exposure. We aimed to provide a concise review of benchmark findings in important neurobiological systems related to the aetiology and maintenance of PTSD symptomology. Specifically, we discuss functional aetiologies in the noradrenergic, serotonergic, endogenous cannabinoid and opioid systems as well as the hypothalamic-pituitary adrenal (EPA) axis. This article provides a succinct framework to appreciate the current understanding of neurobiological mechanisms related to the pathophysiology of PTSD and how these findings may impact the development of future, targeted pharmacological treatments for this debilitating disorder.
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