Welcome to the EPA 2022 Interactive Programme
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"Adding new Molecular Insights to a given Endophenotype: the Relevance of Epigenetics in Environmental Stress Response”
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Molecular psychiatry research needs a deeper characterization of emotional and cognitive neural underpinnings, along with a broader recognition of trauma-related circuitries and their involvement in shared pathological endophenotypes. One such endophenotype is unbalanced approach avoidance conflict (AAC), a highly recurrent trait of psychopathology. A translationally validated rodent model of AAC is the elevated plus maze (EPM) test, recently shown to be pharmacologically controlled in human and rodents via homologous neural substrates. Thanks to this test, we identified the involvement of the epigenetic enzyme LSD1 as a molecular restrainer of anxiety. We identified LSD1 aberrant regulation within the hippocampus of suicidal victims, suggesting its broad functional involvement in maladaptive behaviors. Interestingly, thanks to the parallel employment of rodent models, we evaluated a stress-related LSD1 homeostatic regulation that transiently limits memory formation-instrumental gene expression in the hippocampus upon trauma. Our work shed new light on epigenetic processes devoted to trauma resiliency through a negative regulation of anxiety plasticity.
“Neural Network Responses to Traumatic Stress Predicting its Longterm Consequences"
, Abstract
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Adaptive responding to severe stress or trauma requires an optimized reconfiguration in the activity of large-scale neural networks. In vulnerable individuals, this response can go awry, inducing long-term consequences on mental health, such as posttraumatic stress disorder (PTSD). Improved understanding of the neurobiological mechanisms underlying this maladaptive neural response to trauma might benefit early intervention (i.e., secondary prevention) options in stress-related psychopathology. Yet, because of obvious ethical limitations these acute responses to trauma are inaccessible in humans. Therefore, we here used a mouse model for PTSD to investigate adaptive vs. maladaptive neural responding to trauma, the latter leading to long-term behavioral consequences mimicking symptoms observed in PTSD patients. By using transgenic mice, we were able to fluorescently label all activated neurons during trauma exposure, and relate these activation patterns to later PTSD-like symptomatology. We observed increased neuronal activity in sensory-processing and memory-related areas of mice vulnerable to the long-term consequences of trauma exposure, compared to resilient mice. Moreover, vulnerable mice displayed increased functional connectivity between the default mode network and lateral cortical network (a proxy for the central executive network in humans) during trauma processing relative to resilient mice. As such, these findings provide first insight in how a maladaptive neural response to trauma can result in later symptoms of psychopathology.