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ItemA neuroendocrine study of chronic combat-related post-traumatic stress disorderHOPWOOD, MALCOLM ( 1997)Descriptions of the development of psychiatric symptoms in response to traumatic experience can be found in literature dating back to some of the earliest writings found. Amongst these symptoms there have always been descriptions consistent with what we would now term Post Traumatic Stress Disorder (PTSD). Tomb (1994) describes how such symptoms historically have been most frequently described in relation to combat experience and are contained in such classical texts as Homer’s Iliad. Recognition that such symptoms also occur in association with non combat related trauma is a relatively recent event. This can be seen in description of response to traumas such as The Boston Coconut Grove Fire (Adler 1943) and the Buffalo Creek Dam collapse (Gleser et al 1981). Combined with the massive number of combat veterans with combat experience related to psychiatric disability following the World Wars, significant impetus appears to have developed for separate classification and understanding of trauma related psychiatric symptoms. Together, these forces led to the creation of the diagnostic category of PTSD for the first time in the American Psychiatric Associations DSMIII (APA 1980). In this series of studies, we are thus aiming to further the understanding of the neurobiology of Post Traumatic Stress Disorder by specifically examining a group of male Australian Vietnam veterans with current PTSD, comparing them to two control Vietnam veteran populations, one group of those veterans who previously met criteria for a diagnosis of PTSD and a third group who never have met criteria for a diagnosis of PTSD. We examined these three groups in a number of ways. Firstly, to further understand aspects of central noradrenergic receptor function we utilised a clonidine growth hormone challenge test. Consistent with previous literature on the HPA axis in PTSD from North American we utilised a modified dexamethasone suppression test to investigate feedback within the HPA axis. Finally, we investigated serotonergic receptor function peripherally with a further study of platelet paroxetine binding and performed the first large study examining central serotonergic receptor function using the d-fenfluamine prolactin challenge test. Before describing the methodology and results of these studies I will review relevant findings to these three systems from studies of animal and human models of stress, clinical populations with PTSD and their treatment and previous experimental analysis of relevant biological variables in subjects with PTSD.