ACUTE TRAUMATIC STRESS INDUCES ABNORMAL HIPPOCAMPAL THETA OSCILLATION AND PREDICTS MALADAPTIVE PLASTICITY

Post-traumatic stress disorder (PTSD) imposes a substantial burden on affected individuals, with current treatments providing only partial and variable symptom relief. This has driven growing interest in identifying neurobiological mechanisms that could be targeted for early intervention or prevention after trauma exposure. However, most animal models of PTSD rely on chronic stress paradigms, in which behavioral alterations develop slowly and lack clear temporal anchoring, limiting mechanistic insight. Here, we used high-density silicon probes to characterize physiological responses to an acute traumatic stress experience in hippocampal CA1, a region that consistently shows reduced volume and excitability in human PTSD neuroimaging studies. On the day of the traumatic experience, animals were subjected to 2 hours of immobilization, preceded and followed by 3-hour home-cage recording sessions. We observed that during this single prolonged exposure to traumatic stress, both sexes exhibited sustained theta-band oscillations (4-8 Hz), a rhythm typically associated with exploratory and attentive behaviors and known to gate synaptic plasticity in the hippocampus. Remarkably, pyramidal layer excitability remained significantly elevated days post-immobilization, indicating long-term neurophysiological adaptations following acute traumatic stress. Notably, the magnitude of this elevation was predicted by theta modulation of individual neurons during the stress exposure. In summary a temporally precise traumatic stress model allows to bridge acute physiological responses with chronic vulnerability markers, providing circuit-level insights into PTSD pathogenesis and prevention. Future experiments will address the contributions of specific inhibitory cell populations to these effects, to better understand circuit mechanisms and inform targeted therapeutic strategies.