ACUTE STRESS IMPAIRS LONG-LASTING STORAGE OF AN AVERSIVE MEMORY
Long-lasting storage. Aversive memory. C-fos. Zif268. Acute stress.
Learning and memory are plasticity-related processes guided by our life experiences. Emotions reflect ability to assign valences to those events, making learning of aversive experiences more leaning to persist. Long-lasting storage of a memory is controlled by intracellular signaling cascades activation after learning, which can be modulated by external agents, as stress. Modulation of cognitive functions could be caused by changes at cellular and/or neural levels, through decrease in neurotransmitter release, deactivation of specific kinase pathways, protein synthesis and connectivity damage between limbic brain regions. The aim of our study was to investigate the effect of after training acute stress on the persistence of an aversive memory in rats submitted to avoidance discriminative in elevated plus maze, an apparatus that simultaneously evaluates learning, memory, anxiety and locomotor activity. Our results show that memory lasted up to five days in this task, accompanied by an increase of Zif268 expression in the CA1 sub-region of dorsal hippocampus 18 hours after training. Stress immediately after training diminished long-lasting memory storage and decreased late protein synthesis of Zif268 18 hours after training and C-fos 1 hour after training. The exact mechanism underlying Zif268 and C-fos down-regulation still not clear. However, we suggest that glucocorticoids deregulate MAPK/ERK, JNK and p38MAPK signaling pathways in dorsal hippocampus pyramidal neurons, leading to dysfunctional expression of immediate-early genes.