Post-traumatic stress disorder (PTSD) is a mental disease characterized by distress, disturbing feelings and thoughts regarding the event that caused it, and avoiding syndrome. The identified symptoms are largely associated with such transmitters as serotonin (5-HT), cortisol (COR), norepinephrine (NE), and dopamine (DA). As stated in the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5), during PTSD, 5-HT levels decrease, which is related to amplified aggressiveness and impulsivity (Wilson, Ebenezer, McLaughlin, & Francis, 2014).
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The low levels of 5-HT also make it difficult to regulate excitation, leading to irritability and hypersensitivity, thus causing the excessively emotional response to neutral stimuli. Under chronic stress, the body adapts by increasing negative feedback, which causes an increase in the number of glucocorticoid receptors in the hippocampus, a decrease in the background level of glucocorticoids, and reduction in glucocorticoid synthesis in response to repeated stress stimuli.
The more there are receptors, the more the opportunity to enhance feedback, making ground-glass nodules more sensitive, and allowing one to recover from stress faster. The study by Bandelow et al. (2017) showed that the development of PTSD is associated with the dysregulation of the hypothalamic-pituitary-adrenal axis and the impaired sympathoadrenal medullary system as part of immunity.
In patients with PTSD, low cortisol and high levels of dehydroepiandrosterone (DHEA), necrotic tumor factor (TNF-α), and interleukin-6 (IL-6) were found compared with the healthy control group (Bandelow et al., 2017). With these changes, the authors explain the inflammatory changes accompanying the development of PTSD. As for DA, it is responsible for the reward system of the brain and may be expressed in dopaminergic hyperactivity, when a patient with DTSD becomes unusually energetic, which is rapidly replaced by inertness.
The evidence demonstrates that stress hormones change the structure of the limbic system that involves the hippocampus, one of the most plastic and unstable areas of the brain (Wilson, 2014). In the hippocampus, impulses arrive through ramifications between the dentate gyrus and CA3-pyramidal neurons from the olfactory cortex to the dentate gyrus. Wilson et al. (2014) state that the dentate gyrus is essential in ensuring the memorization of sequences of events, although long-term data storage occurs in other areas of the brain.
Since the CA3 section of the dentate gyrus is balanced and vulnerable, there is adaptive structural plasticity during which new neurons continue to appear throughout life, and pyramidal cells, in response to chronic stress or hibernation, undergo reversible dendritic remodeling. In their study, Depue et al. (2014) suggest that a reduced amygdala is another anatomic change related to PTSD.
At the same time, PTSD causes an increase in physiological parameters, while prolonged stress exposure can lead to pathology. The allostatic overload that exceeds the adaptation threshold leads to atrophy and remodeling of the hippocampal and prefrontal cortex neurons, which are involved in the mechanisms of memory, attention, and executive functions, as well as hypertrophy of neurons almond-shaped nucleus associated with the processes of fear, anxiety, and aggression (Wilson, 2014).
It is especially critical that the stressful experiences of a child, apparently, can occur during the period of active development of the brain. In this period, myelination of its different departments is completed, and neural connections are established, both horizontal (between sections of the cortex) and vertical (between the cortex and subcortical structures), and has a negative effect on the course of these processes. This can lay the foundation for the subsequent development of personality and various affective disorders.
Summarizing behavioral, neuroanatomic, and neurotransmitter changes of PTSD, one may note that the lack of neurotransmitter in neurons of the cortico-basal ganglia-thalamocortical loop, where normally serotonin activity is necessary for inhibiting anxiety, is associated with persistent phobias, anxiety, avoidant behavior, pathological shyness, et cetera (Bandelow et al., 2017). Similarly, an increased level of norepinephrine in the amygdala is associated with the development of nightmarish dreams, obsessive memories, overexcitement, and panic attacks.
In addition, excessive amounts of this neurotransmitter are associated with autonomic disorders such as tachycardia, tremor, hyperventilation, excessive sweating, and so on. The lack of norepinephrine is associated with persistent phobias, nervousness, tension, anxious expectation, and avoiding behavior (Bandelow et al., 2017). Thus, the mentioned neurotransmitters promote processes that ensure the development of anxiety in neurons of cortico-basal ganglia-thalamocortical loops. Based on the mentioned findings, it is possible to suggest that there is a connection between various symptoms of PTSD.
The symptoms that occur as a result of the impaired activity of serotonin and noradrenaline systems are unevenly presented in various diagnostic categories. In other words, the manifestations of anxiety associated with a surplus of norepinephrine are the most characteristic of post-traumatic stress disorder.
Hypothetically, it can be assumed that a decrease in the activity of the GABAergic system is a common and primary pathogenetic mechanism that determines the manifestation of any anxiety disorder, while a specific clinical target depends on the features of metabolic disorders of serotonin and norepinephrine. Most likely, serotonin and norepinephrine neurons try to combat an activity deficit, for example, in the cortico-basal ganglia-thalamocortical loops, thus contributing to better recovery.
Bandelow, B., Baldwin, D., Abelli, M., Bolea-Alamanac, B., Bourin, M., Chamberlain, S. R.,… Grünblatt, E. (2017). Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition. The World Journal of Biological Psychiatry, 18(3), 162-214.
Depue, B. E., Olson-Madden, J. H., Smolker, H. R., Rajamani, M., Brenner, L. A., & Banich, M. T. (2014). Reduced amygdala volume is associated with deficits in inhibitory control: A voxel-and surface-based morphometric analysis of comorbid PTSD/mild TBI. BioMed Research International, 2014, 1-11.
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Wilson, C. B., Ebenezer, P. J., McLaughlin, L. D., & Francis, J. (2014). Predator exposure/psychosocial stress animal model of post-traumatic stress disorder modulates neurotransmitters in the rat hippocampus and prefrontal cortex. PLoS One, 9(2), 1-7.