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Purpose <p>Post-traumatic stress disorder (PTSD) is one of the major mental disorders that arise after experiencing severe traumatic events, but an objective evaluation method using molecular imaging has not yet been developed. Previous research has mainly focused on the chronic aspects of PTSD, making it difficult to assess the acute effects of PTSD. This study aims to evaluate the functional changes in the central nervous system in the early stages of PTSD using positron emission tomography (PET).</p> Procedures <p>We used the single prolonged stress (SPS) protocol to make a PTSD animal model. Female Sprague–Dawley rats were classified into control and SPS groups (<i>n</i> = 6 for each group). The SPS group was sequentially subjected to restraint, forced swimming, and anesthesia stresses. After a quiescent period of 7 days, multiple PET scans were conducted for each animal using specific radiotracers targeting the glutamatergic, gamma-aminobutyric acid (GABA), and serotonergic systems to assess functional neuronal changes. Following the PET scans, histological evaluations were performed in the hippocampus using cresyl violet staining to measure neuronal loss.</p> Results <p>SPS exposure did not result in differences in body weight between the SPS and control groups. In the glutamate PET, the SPS group showed comparable brain uptake to the control group. However, the GABA and serotonin PET for the SPS group showed significantly reduced binding values compared with those of the control group. Specifically, GABA PET showed significant reductions in the cingulate, frontal association, medial prefrontal, and orbitofrontal cortices <i>(p &lt;</i> 0.01). Serotonin PET showed decreased brain uptake in the amygdala, cortex, and hippocampus. Following the imaging study, histological analysis across the hippocampus, cortex, and amygdala revealed a significant reduction in neuronal density only in the CA2 region of the hippocampus in the SPS group (<i>p</i> &lt; 0.01); however, no significant changes were observed in the other examined areas.</p> Conclusions <p>Evaluating the acute effects of PTSD showed that it does not affect body weight but has a considerable impact on specific neuronal circuits, including GABAergic and serotonergic systems. These findings suggest that the GABA and serotonin systems may be key targets in the early phase of PTSD.</p>

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The Early Stage of post-traumatic Stress Disorder (PTSD) Event Induces Down-Regulation of the Gamma-Aminobutyric Acidergic- Serotonergic System: Multiple PET Imaging in a PTSD Animal Model

  • 期刊论文

  • 发表日期：

    2025年12月15日

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  • Bo Hyun Kim,
  • Se Jong Oh,
  • Namhun Lee,
  • Jong Hee Choi,
  • Kyung Rok Nam,
  • Kyung Jun Kang,
  • Sang Jin Han,
  • Jae Yong Choi

摘要

Purpose

Post-traumatic stress disorder (PTSD) is one of the major mental disorders that arise after experiencing severe traumatic events, but an objective evaluation method using molecular imaging has not yet been developed. Previous research has mainly focused on the chronic aspects of PTSD, making it difficult to assess the acute effects of PTSD. This study aims to evaluate the functional changes in the central nervous system in the early stages of PTSD using positron emission tomography (PET).

Procedures

We used the single prolonged stress (SPS) protocol to make a PTSD animal model. Female Sprague–Dawley rats were classified into control and SPS groups (n = 6 for each group). The SPS group was sequentially subjected to restraint, forced swimming, and anesthesia stresses. After a quiescent period of 7 days, multiple PET scans were conducted for each animal using specific radiotracers targeting the glutamatergic, gamma-aminobutyric acid (GABA), and serotonergic systems to assess functional neuronal changes. Following the PET scans, histological evaluations were performed in the hippocampus using cresyl violet staining to measure neuronal loss.

Results

SPS exposure did not result in differences in body weight between the SPS and control groups. In the glutamate PET, the SPS group showed comparable brain uptake to the control group. However, the GABA and serotonin PET for the SPS group showed significantly reduced binding values compared with those of the control group. Specifically, GABA PET showed significant reductions in the cingulate, frontal association, medial prefrontal, and orbitofrontal cortices (p < 0.01). Serotonin PET showed decreased brain uptake in the amygdala, cortex, and hippocampus. Following the imaging study, histological analysis across the hippocampus, cortex, and amygdala revealed a significant reduction in neuronal density only in the CA2 region of the hippocampus in the SPS group (p < 0.01); however, no significant changes were observed in the other examined areas.

Conclusions

Evaluating the acute effects of PTSD showed that it does not affect body weight but has a considerable impact on specific neuronal circuits, including GABAergic and serotonergic systems. These findings suggest that the GABA and serotonin systems may be key targets in the early phase of PTSD.