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Edut, S.

Publications and source records attributed to Edut, S..

2 recordsLinked to original sources

Prefrontal Control of Innate Escape Behavior - A Neural Mechanism of Enhanced Posttraumatic Threat Detection

Innate defensive responses, while primarily instinctive, must also be flexible and highly adaptive to changes in risk assessment. As such, efficient innate escape behavior requires intricate processing to minimize reaction time while maximizing the success and adaptivity of the action. The superior colliculus (SC) is a subcortical sensorimotor integration center linking sensory threat information and escape. Adaptive changes in innate escape after learning could take a maladaptive turn after severe stress. Posttraumatic stress disorder (PTSD) is associated with long-term maladaptive changes after exposure to traumatic events, related to enhanced threat detection and reaction. Such long-term modifications are thought to involve the medial prefrontal cortex (mPFC), which is implicated in integrating learned emotional values into decisions that drive actions and behaviors. Here, in a series of experiments, we establish the crucial physiological role of specific mPFC neurons, exerting influence on the SC both directly and indirectly through the basal ganglia, in threat detection and reaction after adversity.

neuroscience↗

The role of hippocampal CaMKII in resilience to trauma-related psychopathology

Traumatic stress exposure can form persistent trauma-related memories. However, only a minority of individuals develop post-traumatic stress disorder (PTSD) symptoms upon exposure. We employed a rat model of PTSD, which enables differentiating between exposed-affected and exposed-unaffected individuals. Two weeks after the end of exposure, animals were tested behaviorally, following an exposure to a trauma reminder, identifying them as trauma affected or unaffected. In light of the established role of hippocampal synaptic plasticity in stress and the essential role of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in hippocampal based synaptic plasticity, in two separate experiments, we pharmacologically inhibited CaMKII or knocked-down CaMKII in the dorsal dentate gyrus of the hippocampus (dDG) following exposure to the same trauma paradigm. Both manipulations brought down the prevalence of affected individuals in the trauma- exposed population. A day after the last behavioral test, long-term potentiation (LTP) was examined in the dDG as a measure of synaptic plasticity. Trauma exposure reduced the ability to induce LTP, whereas, contrary to expectation, CaMKII-kd reversed this effect. Further examination revealed that reducing CaMKII expression, enables the formation of CaMKII-independent LTP, which may enable increased resilience in the face of a traumatic experience. The current findings further emphasize the pivotal role dDG has in stress resilience.

neuroscience↗