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Abstract
Post-traumatic stress disorder (PTSD) afflicts approximately 8% of the United States population and represents a significant public health burden, but the underlying neural mechanisms of this and other anxiety- and stressor-related disorders are largely unknown. Within the last few decades, several preclinical models of PSTD have been developed to help elucidate the mechanisms underlying dysregulated fear states. One brain area that has emerged as a critical mediator of stress-related behavioral processing in both clinical and laboratory settings is the bed nucleus of the stria terminalis (BNST). The BNST is interconnected with essential emotional processing regions, including prefrontal cortex, hippocampus and amygdala. It is activated by stressor exposure and undergoes neurochemical and morphological alterations as a result of stressor exposure. Stress-related neuro-peptides including corticotropin-releasing factor (CRF) and pituitary adenylate cyclase activating peptide (PACAP) are also abundant in the BNST, further implicating an involvement of BNST in stress responses. Behaviorally, the BNST is critical for acquisition and expression of fear and is well positioned to regulate fear relapse after periods of extinction. Here, we consider the role of the BNST in stress and memory processes in the context of preclinical models of PTSD.
Highlights
Stress-related disorders, such as post-traumatic stress disorder (PTSD), are among the most debilitating neuropsychopathologies in the world
There has been a considerable effort in the past several years to understand the neural mechanisms underlying acquisition of fear responses in animal models (Goode and Maren, 2017), in regions associated with behavioral responses to stressor exposure
We begin this review by discussing the differences between amygdala and bed nucleus of the stria terminalis (BNST) as they relate to Post-traumatic stress disorder (PTSD)
Summary
Stress-related disorders, such as post-traumatic stress disorder (PTSD), are among the most debilitating neuropsychopathologies in the world. Rodents are evaluated based on whether their behavioral changes following stressor exposure match a PTSD phenotype in humans after trauma (despite differences in motivation, emotion, and cognition between rodents and humans; for review, see Lezak et al, 2017), and whether these changes can be attenuated by medications used to treat stress-related disorders Using this approach, early studies identified several brain regions, including the bed nucleus of the stria terminalis (BNST) and the amygdala, that are highly involved in mediating PTSD-like behaviors in rodents. We consider current animal models of PTSD, critically review the specific involvement of BNST in each, and discuss the neural mechanisms driving behavioral manifestations of fear-related pathologies like PTSD Based on these ideas, and a growing literature in BNST research, we suggest a critical role of BNST in PTSD-related behaviors and recommend continued research to explain how neural circuits involved in stress processing become dysregulated, and stay dysregulated, in response to trauma
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