The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib

The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice (GRNesCre), we identified synapsin-Ia/Ib as one of the effectors of the glucocorticoid signaling cascade. Stress and glucocorticoid-induced activation of the GR modulate synapsin-Ia/Ib through two complementary mechanisms. First, glucocorticoids driving Egr-1 expression increase the expression of synapsin-Ia/Ib, and second, glucocorticoids driving MAPK activation increase its phosphorylation. Finally, we showed that blocking fucosylation of synapsin-Ia/Ib in the hippocampus inhibits its expression and prevents the glucocorticoid-mediated increase in stress-related memory. In conclusion, our data provide a complete molecular pathway (GR/Egr-1/MAPK/Syn-Ia/Ib) through which stress and glucocorticoids enhance the memory of stress-related events and highlight the function of synapsin-Ia/Ib as molecular effector of the behavioral effects of stress

Post-training intra-hippocampal infusions of corticosterone promote, preserve or disrupt conditioned fear responses depending on the streesful situation

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Glucocorticoids can induce PTSD-like memory impairments in mice

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BDNF-TrkB signaling through Erk1/2MAPK phosphorylation mediates the enhancement of fear memory induced by glucocorticoids

International audienceActivation of glucocorticoid receptors (GR) by glucocorticoid hormones (GC) enhances contextual fear memories through the activation of the Erk1/2(MAPK) signaling pathway. However, the molecular mechanism mediating this effect of GC remains unknown. Here we used complementary molecular and behavioral approaches in mice and rats and in genetically modified mice in which the GR was conditionally deleted (GR(NesCre)). We identified the tPA-BDNF-TrkB signaling pathway as the upstream molecular effectors of GR-mediated phosphorylation of Erk1/2(MAPK) responsible for the enhancement of contextual fear memory. These findings complete our knowledge of the molecular cascade through which GC enhance contextual fear memory and highlight the role of tPA-BDNF-TrkB-Erk1/2(MAPK) signaling pathways as one of the core effectors of stress-related effects of GC

Stress modulates instrumental learning performances in horses (Equus caballus) in interaction with temperament

The present study investigates how the temperament of the animal affects the influence of acute stress on the acquisition and reacquisition processes of a learning task. After temperament was assessed, horses were subjected to a stressor before or after the acquisition session of an instrumental task. Eight days later, horses were subjected to a reacquisition session without any stressor. Stress before acquisition tended to enhance the number of successes at the beginning of the acquisition session. Eight days later, during the reacquisition session, contrary to non-stressed animals, horses stressed after acquisition, and, to a lesser extent, horses stressed before acquisition, did not improve their performance between acquisition and reacquisition sessions. Temperament influenced learning performances in stressed horses only. Particularly, locomotor activity improved performances whereas fearfulness impaired them under stressful conditions. Results suggest that direct exposure to a stressor tended to increase acquisition performances, whereas a state of stress induced by the memory of a stressor, because it has been previously associated with the learning context, impaired reacquisition performances. The negative effect of a state of stress on reacquisition performances appeared to be stronger when exposure to the stressor occurred after rather than before the acquisition session. Temperament had an impact on both acquisition and reacquisition processes, but under stressful conditions only. These results suggest that stress is necessary to reveal the influence of temperament on cognitive performances