Abstract
A highly conserved network of brain structures regulates the expression of fear and anxiety in mammals. Many of these structures display abnormal activity levels in post-traumatic stress disorder (PTSD). However, some of them, like the bed nucleus of the stria terminalis (BNST) and amygdala, are comprised of several small sub-regions or nuclei that cannot be resolved with human neuroimaging techniques. Therefore, we used a well-characterized rat model of PTSD to compare neuronal properties in resilient vs PTSD-like rats using patch recordings obtained from different BNST and amygdala regions in vitro. In this model, a persistent state of extreme anxiety is induced in a subset of susceptible rats following predatory threat. Previous animal studies have revealed that the central amygdala (CeA) and BNST are differentially involved in the genesis of fear and anxiety-like states, respectively. Consistent with these earlier findings, we found that between resilient and PTSD-like rats were marked differences in the synaptic responsiveness of neurons in different sectors of BNST and CeA, but whose polarity was region specific. In light of prior data about the role of these regions, our results suggest that control of fear/anxiety expression is altered in PTSD-like rats such that the influence of CeA is minimized whereas that of BNST is enhanced. A model of the amygdalo-BNST interactions supporting the PTSD-like state is proposed.
Highlights
Convergent findings from animal and human studies implicate a highly conserved network of brain structures in the expression of fear and anxiety.[1]
These results suggest that differences in the potency of stria terminalis (ST)-evoked inhibition contribute to reduce the orthodromic responsiveness of bed nucleus of the stria terminalis (BNST)-AL neurons in post-traumatic stress disorder (PTSD)-like relative to resilient rats
Using patch recordings in brain slices kept in vitro, we studied the intrinsic and synaptic responsiveness of BNST and amygdala neurons in a rat model of PTSD
Summary
Convergent findings from animal and human studies implicate a highly conserved network of brain structures in the expression of fear and anxiety.[1]. PTSD is characterized by a fear extinction deficit that develops after trauma[8] and a hippocampaldependent allocentric spatial processing deficit that predates trauma.[9,10] The Lewis rat model of PTSD reproduces these two deficits, including their different temporal relationship to trauma.[5,11,12]. Using this model, we compared the intrinsic and synaptic responsiveness of BNST and amygdala neurons in resilient vs susceptible rats with patch recordings in vitro. This approach revealed that the PTSD-like state is associated with distributed but region-specific alterations in the synaptic responsiveness of BNST and amygdala neurons
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