Modulation of neuroplasticity-related targets following stress-induced acute escape deficit

Publication date: Available online 13 February 2019

Source: Behavioural Brain Research

Author(s): C. Benatti, G. Radighieri, S. Alboni, J.M.C. Blom, N. Brunello, F. Tascedda

Abstract

Understanding resilience is a major challenge to improve current pharmacological therapies aimed at complementing psychological-based approaches of stress-related disorders. In particular, resilience is a multi-factorial construct where the complex network of molecular events that drive the process still needs to be resolved. Here, we exploit the Acute Escape Deficit model, an animal model based on exposure to acute unavoidable stress followed by an escape test, to define vulnerable and resilient phenotypes in rats. Hippocampus and prefrontal cortex (PFC), two of the brain areas most involved in the stress response, were analysed for gene expression at two different time points (3 and 24 hours) after the escape test. Total brain-derived neurotrophic factor (BDNF) was highly responsive in the PFC at 24-hour after the escape test, while expression of BDNF transcript IV increased in the hippocampus of resistant animals 3 hours post-test. Expression of memory enhancers like Neuronal PAS Domain Protein 4 (Npas4) and Activity-regulated cytoskeleton-associated protein (Arc) decreased in a time- and region-dependent fashion in both behavioural phenotypes. Also, the memory inhibitor Protein Phosphatase 1 (Ppp1ca) was increased in the hippocampus of resilient rats at 3 hours post-test. Given the importance of neurotrophic factors and synaptic plasticity-related genes for the development of appropriate coping strategies, our data contribute to an additional step forward in the comprehension of the psychobiology of stress and resiliency.

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