Abstract
Post-Traumatic Stress Disorder (PTSD) can develop in response to a traumatic event involving a threat to life. To date, no diagnostic biomarkers have been identified for PTSD. Recent research points toward physiological abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, sympathoadrenal medullary and immune system that may be implicated in the disorder. The modulation of neurotransmitters is another possible mechanism, but their role in the progression of PTSD is poorly understood. Low serotonin (5-HT) may be a factor, but it may not be the only neurotransmitter affected as modulation affects levels of other neurotransmitters. In this study, we hypothesized the predator exposure/psychosocial stress rodent model of PTSD may alter levels of 5-HT and other neurotransmitters in the rat hippocampus and prefrontal cortex (PFC). Male Sprague-Dawley rats were used in this experiment. We induced PTSD via a predator exposure/psychosocial stress model, whereby rats were placed in a cage with a cat for 1 hour on days 1 and 11 of the 31-day experiment. Rats also received psychosocial stress via daily cage cohort changes. On day 32, the rats were sacrificed and the brains dissected to remove the hippocampus and PFC. Norepinephrine (NE), 5-Hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), dopamine (DA), and 3,4-Dihydroxyphenylacetic acid (DOPAC), and 5-HT levels in the hippocampus and PFC were measured with high-performance liquid chromatography (HPLC). In the hippocampus, 5-HT and HVA were lower, while NE and DOPAC were higher, in the PTSD group vs. controls. In the PFC, only 5-HT was lower, while NE, DA, and DOPAC were higher, in the PTSD group vs. controls. The rate limiting enzymes tyrosine hydroxylase and tryptophan hydroxylase were also examined and confirmed our findings. These results demonstrate that the predator exposure/psychosocial stress model of PTSD produces neurotransmitter changes similar to those seen in human patients and may cause a heightened noradrenergic response.
Highlights
Post-Traumatic Stress Disorder (PTSD), recently reclassified as a trauma- and stressor-related disorder, can develop in response to real or perceived life-threatening situations
Statistical analyses were performed using Prism (GraphPad Software, Inc; version 5.0). Neurotransmitters and their Metabolites were Modulated in the Hippocampus and prefrontal cortex (PFC)
To investigate the influence of the predator exposure/psychosocial stress regimen on neurotransmitter modulation, we examined endogenous levels of biogenic amines and their metabolites in the hippocampus and PFC of control and PTSD animals using high-performance liquid chromatography (HPLC)
Summary
Post-Traumatic Stress Disorder (PTSD), recently reclassified as a trauma- and stressor-related disorder, can develop in response to real or perceived life-threatening situations. According to the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5), a diagnosis of PTSD necessitates exposure to a life-threatening event, intrusive recollections of the event, avoidance of associated stimuli and numbing of general responsiveness, negative cognitions/mood, hyperarousal not present before the trauma, and a significant social impairment. All of these symptoms must persist for at least 30 days and not be due to illness, medication, or substance abuse [1]. Exactly which neurotransmitters are up- or downregulated during PTSD progression
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