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

Revest, Jean‐Michel; Roux, A Le; Roullot-Lacarrière, Valérie; Kaouane, Nadia; Vallée, Monique; Kasanetz, Fernando; Rougé‐Pont, Françoise; Tronche, François; Desmedt, Aline; Piazza, Pier-Vincenzo

doi:10.1038/mp.2013.134

Cited by 120 publications

(103 citation statements)

References 92 publications

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“…Because corticosterone (CORT), the main stress hormone in rodents, was shown to enhance the consolidation of adaptive fear memory in some stressful situations (Phelps, 2004;Quirarte et al, 1997;Revest et al, 2005Revest et al, , 2010Revest et al, , 2014, but also to impair the hippocampal function and disrupt context-based memory in others (Bremner et al, 2004;de Kloet et al, 2005;Sapolsky, 1996), we hypothesized that injections of CORT into the hippocampus, its main brain target, immediately after fear conditioning might either promote adaptive or produce PTSD-like fear memory as a function of the intensity of the stressful event. In order to observe a putative experimental bias toward a cue-based memory at the expense of a hippocampal-dependent context-based memory of the trauma, we used a predicting-context condition in which a discrete (tone) CS is present but irrelevant (not predictive of the US).…”

Section: Hippocampal-amygdalar Interaction Qualify Emotional Memory Rmentioning

confidence: 99%

Adaptive emotional memory: the key hippocampal–amygdalar interaction

Desmedt

Marighetto

Richter‐Levin

et al. 2015

Stress

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For centuries philosophical and clinical studies have emphasized a fundamental dichotomy between emotion and cognition, as, for instance, between behavioral/emotional memory and explicit/representative memory. However, the last few decades cognitive neuroscience have highlighted data indicating that emotion and cognition, as well as their underlying neural networks, are in fact in close interaction. First, it turns out that emotion can serve cognition, as exemplified by its critical contribution to decision-making or to the enhancement of episodic memory. Second, it is also observed that reciprocally cognitive processes as reasoning, conscious appraisal or explicit representation of events can modulate emotional responses, like promoting or reducing fear. Third, neurobiological data indicate that reciprocal amygdalar-hippocampal influences underlie such mutual regulation of emotion and cognition. While supporting this view, the present review discusses experimental data, obtained in rodents, indicating that the hippocampal and amygdalar systems not only regulate each other and their functional outcomes, but also qualify specific emotional memory representations through specific activations and interactions. Specifically, we review consistent behavioral, electrophysiological, pharmacological, biochemical and imaging data unveiling a direct contribution of both the amygdala and hippocampal-septal system to the identification of the predictor of a threat in different situations of fear conditioning. Our suggestion is that these two brain systems and their interplay determine the selection of relevant emotional stimuli, thereby contributing to the adaptive value of emotional memory. Hence, beyond the mutual quantitative regulation of these two brain systems described so far, we develop the idea that different activations of the hippocampus and amygdala, leading to specific configurations of neural activity, qualitatively impact the formation of emotional memory representations, thereby producing either adaptive or maladaptive fear memories.

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Section: Hippocampal-amygdalar Interaction Qualify Emotional Memory Rmentioning

confidence: 99%

Adaptive emotional memory: the key hippocampal–amygdalar interaction

Desmedt

Marighetto

Richter‐Levin

et al. 2015

Stress

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“…Enhanced memory formation may involve BDNF-TrkB-MAPK-synapsin Ia/Ib signaling (Revest et al 2005(Revest et al , 2010(Revest et al , 2014 and CaMKII-BDNF-CREB signaling (Chen et al 2012). Yet, it remains to be determined how corticosteroid hormones regulate synaptic function, which is fundamental for memory formation (Rumpel et al 2005;Kessels and Malinow 2009).…”

Section: Discussionmentioning

confidence: 99%

mTOR is essential for corticosteroid effects on hippocampal AMPA receptor function and fear memory

et al. 2015

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Glucocorticoid hormones, via activation of their receptors, promote memory consolidation, but the exact underlying mechanisms remain elusive. We examined how corticosterone regulates AMPA receptors (AMPARs), which are crucial for synaptic plasticity and memory formation. Combining a live imaging fluorescent recovery after photobleaching approach with the use of the pH-sensitive GFP-AMPAR tagging revealed that corticosterone enhances the AMPAR mobile fraction and increases synaptic trapping of AMPARs in hippocampal cells. In parallel, corticosterone-enhanced AMPARmediated synaptic transmission. Blocking the mammalian target of rapamycin (mTOR) pathway prevented the effects of corticosterone on both AMPAR trapping-but not on the mobile fraction-and synaptic transmission. Blocking the mTOR pathway also prevented the memory enhancing effects of corticosterone in a contextual fear-conditioning paradigm. We conclude that activation of the mTOR pathway is essential for the effects of corticosterone on synaptic trapping of AMPARs and, possibly as a consequence, fearful memory formation.

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“…Results of previous studies have indicated that BDNF activates MAP kinase and Akt signaling pathways (Chen et al 2013, Revest et al 2014. Therefore, we examined the role of Akt and MAP kinase in HO-1 activation.…”

Section: Bdnf-directed Colon Cancer Cell Migration Involves Vegf Exprmentioning

confidence: 99%

Brain-derived neurotrophic factor regulates cell motility in human colon cancer

Huang¹,

Lin²,

Lin³

et al. 2015

Endocrine-Related Cancer

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Brain-derived neurotrophic factor (BDNF) is a potent neurotrophic factor that has been shown to affect cancer cell metastasis and migration. In the present study, we investigated the mechanisms of BDNF-induced cell migration in colon cancer cells. The migratory activities of two colon cancer cell lines, HCT116 and SW480, were found to be increased in the presence of human BDNF. Heme oxygenase-1 (HO)-1 is known to be involved in the development and progression of tumors. However, the molecular mechanisms that underlie HO-1 in the regulation of colon cancer cell migration remain unclear. Expression of HO-1 protein and mRNA increased in response to BDNF stimulation. The BDNF-induced increase in cell migration was antagonized by a HO-1 inhibitor and HO-1 siRNA. Furthermore, the expression of vascular endothelial growth factor (VEGF) also increased in response to BDNF stimulation, as did VEGF mRNA expression and transcriptional activity. The increase in BDNF-induced cancer cell migration was antagonized by a VEGF-neutralizing antibody. Moreover, transfection with HO-1 siRNA effectively reduced the increased VEGF expression induced by BDNF. The BDNF-induced cell migration was regulated by the ERK, p38, and Akt signaling pathways. Furthermore, BDNF-increased HO-1 and VEGF promoter transcriptional activity were inhibited by ERK, p38, and AKT pharmacological inhibitors and dominantnegative mutants in colon cancer cells. These results indicate that BDNF increases the migration of colon cancer cells by regulating VEGF/HO-1 activation through the ERK, p38, and PI3K/Akt signaling pathways. The results of this study may provide a relevant contribution to our understanding of the molecular mechanisms by which BDNF promotes colon cancer cell motility.

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

Cited by 120 publications

References 92 publications

Adaptive emotional memory: the key hippocampal–amygdalar interaction

Adaptive emotional memory: the key hippocampal–amygdalar interaction

mTOR is essential for corticosteroid effects on hippocampal AMPA receptor function and fear memory

Brain-derived neurotrophic factor regulates cell motility in human colon cancer

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