Krystal JH, Neumeister A. Noradrenergic and serotonergic mechanisms in the neurobiology of posttraumatic stress disorder and resilience. Brain Res 1293: 13-23

Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06516, USA.
Brain research (Impact Factor: 2.84). 04/2009; 1293:13-23. DOI: 10.1016/j.brainres.2009.03.044
Source: PubMed


Posttraumatic stress disorder (PTSD) is characterized mainly by symptoms of re-experiencing, avoidance and hyperarousal as a consequence of catastrophic and traumatic events that are distinguished from ordinary stressful life events. Although extensive research has already been done, the etiology of PTSD remains unclear. Research on the impact of trauma on neurobiological systems can be expected to inform the development of treatments that are directed specifically to symptoms of PTSD. During the past 25 years there has been a dramatic increase in the knowledge about noradrenergic and serotonergic mechanisms in stress response, PTSD and more recently in resilience and this knowledge has justified the use of antidepressants with monoaminergic mechanisms of action for patients with PTSD. Nevertheless, available treatments of PTSD are only to some extent effective and enhanced understanding of the neurobiology of PTSD may lead to the development of improved treatments for these patients. In the present review, we aim to close existing gaps between basic research in psychopathology, neurobiology and treatment development with the ultimate goal to translate basic research into clinically relevant findings which may directly benefit patients with PTSD.

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    • "The misin - terpretations of emotional stimuli that occur with PTSD accompany decreased serotonin levels ; decreased serotonin further increases activation of the amygdala . Increases in serotonin intake , however , have the effect of decreasing the threshold for amygdala reactivity ( Krystal & Neumeister , 2009 ) . Optimism is the anticipation of positive outcomes from events and therefore is an important coping strategy that can reinforce stress resistance in individuals who have expe - rienced trauma ( Feder et al . "
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    ABSTRACT: The Check (“Check, Change What You Need To Change and/or Keep What You Want”) art therapy protocol is a sequence of directives for treating trauma that is grounded in neurobiological theory and designed to facilitate trauma narrative processing, autobiographical coherency, and the rebalancing of dysregulated responses to psychosocial stressors and trauma impacts. This article reviews the neurobiological systems involved in trauma processing and demonstrates the Check protocol with the case of a woman with posttraumatic stress disorder who had witnessed the September 11, 2001, attacks on the World Trade Center in New York, New York. A comparison of pre- and post-treatment assessments showed decreased anxiety and avoidance behaviors and improved resiliency.
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    • "Early and adequately dosed exogenous opiates after traumatic burns,42,43 serious trauma-related injuries,44 and during intensive care treatment45 may probably mediate a secondary preventive efficacy with respect to later PTSD risk. It still has to be investigated whether early applied opiates may deliver a general prophylactic effect regarding later PTSD beyond this special pain-related effect.46 "
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    ABSTRACT: Post-traumatic stress disorder (PTSD) may be associated with long-lasting psychological suffering, distressing psychosocial disability, markedly reduced health-related quality of life, and increased morbidity and mortality in a subgroup of individuals in the aftermath of serious traumatic events. Both etiopathogenesis and treatment modalities of PTSD are best conceptualized within a biopsychosotial model. Pharmacotherapy may lay claim to a major role in the multimodal treatment approaches. Here we outline two different pharmacotherapeutic trends that aim to modify the encoding, consolidation, and rehearsal of traumatic memory in order to reduce the risk of PTSD immediately after trauma exposure on the one hand, and that endeavor to treat the clinical state of PTSD on the other. The theoretical rationales of both pharmacological strategies are the complex neurobiological underpinnings that characterize traumatic memory organization and clinical PTSD. Meanwhile, promising data from randomized controlled trials have been obtained for both approaches. Empirical evidence may inform clinicians in their clinical efforts for this special group of patients. The efficacy of several classes of drugs that have been investigated within a context of research should be evaluated critically and still have to stand the test of effectiveness in daily clinical practice. From a patient perspective, empirical results may serve as a psychoeducative guideline to what pharmacotherapeutic approaches may realistically achieve, what their risks and benefits are, and what their limits are in contributing to reducing the often major chronic suffering caused by serious traumatic events. Ethical issues have to be considered, particularly in the context of pharmacological strategies projected to prevent PTSD in the aftermath of traumatic exposure.
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    • "However, chronic exposure to stressors is a risk factor for developing a range of mental health disorders such as anxiety and depression (Friedmann et al., 2006; Itoi and Sugimoto, 2010). The precise mechanisms underlying the adaptive or resilience responses to stressors compared to those which manifest in deleterious consequences remain elusive (Krystal and Neumeister, 2009; Russo et al., 2012). "
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    ABSTRACT: The locus coeruleus (LC) nucleus modulates adaptive behavioral responses to stress and dysregulation of LC neuronal activity is implicated in stress-induced mental illnesses. The LC is composed primarily of noradrenergic neurons together with various glial populations. A neuroglia cell-type largely unexplored within the LC is the NG2 cell. NG2 cells serve primarily as oligodendrocyte precursor cells throughout the brain. However, some NG2 cells are in synaptic contact with neurons suggesting a role in information processing. The aim of this study was to neurochemically and anatomically characterize NG2 cells within the rat LC. Furthermore, since NG2 cells have been shown to proliferate in response to traumatic brain injury, we investigated whether such NG2 cells plasticity also occurs in response to emotive insults such as stress. Immunohistochemistry and confocal microscopy revealed that NG2 cells were enriched within the pontine region occupied by the LC. Close inspection revealed that a sub-population of NG2 cells were located within unique indentations of LC noradrenergic somata and were immunoreactive for the neuronal marker NeuN whilst NG2 cell processes formed close appositions with clusters immunoreactive for the inhibitory synaptic marker proteins gephyrin and the GABA-A receptor alpha3-subunit, on noradrenergic dendrites. In addition, LC NG2 cell processes were decorated with vesicular glutamate transporter 2 immunoreactive puncta. Finally, 10 days of repeated restraint stress significantly increased the density of NG2 cells within the LC. The study demonstrates that NG2 IR cells are integral components of the LC cellular network and they exhibit plasticity as a result of emotive challenges.
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