Stress is known to have a critical impact on memory processes. In the present work, we focus on the effects of an acute stress event closely associated to an unrelated learning task. Here, we show that acute stress (elevated platform [EP] session) experienced 1 hr after a weak spatial object recognition (SOR) training, which only induces a short‐term memory (STM), promoted the formation of SOR‐long term memory (SOR‐LTM) in rats. The effect induced by stress was dependent on the activation of glucocorticoid‐ and mineralocorticoid‐receptors, brain‐derived neurotrophic factor (BDNF) and protein synthesis in the dorsal hippocampus. In contrast, EP after a strong SOR impaired SOR‐LTM probably by interfering with the use of necessary resources. Moreover, we show that the EP session before training induced anterograde interference, which it was not reversed by a subsequent exposure to an open field. Our findings provide novel insights into the impact of stress on LTM formation in rodents and they are discussed under the behavioral analogue of the synaptic tagging and capture hypothesis.
the superiority of spaced over massed learning is an established fact in the formation of longterm memories (LtM). Here we addressed the cellular processes and the temporal demands of this phenomenon using a weak spatial object recognition (wSoR) training, which induces short-term memories (StM) but not LtM. We observed SoR-LtM promotion when two identical wSoR training sessions were spaced by an inter-trial interval (ITI) ranging from 15 min to 7 h, consistently with spaced training. The promoting effect was dependent on neural activity, protein synthesis and ERKs1/2 activity in the hippocampus. Based on the "behavioral tagging" hypothesis, which postulates that learning induces a neural tag that requires proteins to induce LtM formation, we propose that retraining will mainly retag the sites initially labeled by the prior training. thus, when weak, consecutive training sessions are experienced within an appropriate spacing, the intracellular mechanisms triggered by each session would add, thereby reaching the threshold for protein synthesis required for memory consolidation. Our results suggest in addition that ERKs1/2 kinases play a dual role in SOR-LTM formation after spaced learning, both inducing protein synthesis and setting the SoR learning-tag. Overall, our findings bring new light to the mechanisms underlying the promoting effect of spaced trials on LtM formation.
Stress is used to describe physiological and behavioral changes elicited by events that are interpreted as threatening or challenging to an individual (McEwen, 2000;Ness & Calabrese, 2016). Several substances are released in response to stressful events, as glucocorticoids and noradrenaline, which act over numerous neural networks enabling organisms to successfully cope with the stressor (Joëls & Baram, 2009;McIntyre et al., 2012). Diverse brain areas as
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