Recent Progress in Understanding the Pathophysiology of Post-Traumatic Stress Disorder

Abstract

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 (HPA) 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.

Enhanced noradrenergic activity in the amygdala contributes to hyperarousal in an animal model of PTSD

“…Alternatively, the effects of a hypernoradrenergic state in the amygdala could be mediated by β1-adrenoreceptors since propranolol is a nonselective beta blocker. Also, an increased activity of other neurotransmitter systems in the amygdala such as the serotoninergic projections from the raphe (Bailey et al, 2013;Hendriksen et al, 2014;Pitman et al, 2012) might be necessary for the expression of hyperarousal symptoms.…”

“…Therefore, we evaluated the mRNA levels of β1-and β2-adrenergic receptors in the amygdala. Previous studies have shown that the alteration in the activity of the circuit prefrontal cortexhippocampus-amygdala is involved in the pathophysiology of PTSD (Bailey et al, 2013;Hendriksen et al, 2014;Pitman et al, 2012). Thus, we evaluated the expression of the β-adrenergic receptors in these three areas of the brain (see table 2).…”

A SYSTEMATIC REVIEW OF TUMOR NECROSIS FACTOR-α IN POST-TRAUMATIC STRESS DISORDER: EVIDENCE FROM HUMAN AND ANIMAL STUDIES

“…The type and duration of trauma, psychological factors like personality characteristics, gender, and biological factors all seem to play a significant role in PTSD aetiology (Yehuda et al 1995, Breslau et al 1997, Frans et al 2005). Several mechanisms have been implicated in the pathophysiology of PTSD including genetics, epigenetics, and neurobiological systems (Pitman et al 2012, Bailey et al 2013, Ryan et al 2016. Recently, PTSD research has focused on immune mechanisms, for example, peripheral blood mononuclear cells (PBMCs) and cytokines, such as tumor necrosis factor-alpha (TNF-; Andrews & Neises 2012).…”

Transient outwardly rectifying A currents are involved in the firing rate response to altered CO2 in chemosensitive locus coeruleus neurons from neonatal rats

“…One such region that contains a large percentage of chemosensitive neurons is the locus coeruleus (LC). The LC is an important noradrenergic region in the pons and has been implicated to play a role in many pathological conditions, including panic disorder, Rett syndrome, and posttraumatic stress disorder (1,55,65,66). In addition, chemosensitive LC neurons are believed to be a part of a distributed network of neurons that are involved in the control of breathing (18,35).…”