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Séminaire - Cristina Alberini Mechanisms underlying long-term memory: growth in response to stress

Abstract :

Ce séminaire SFR  se tiendra  le Mardi 27 Mai 2014 à la place du vendredi 30 Mai .

 It is well known that emotionally important events are well remembered and that arousal and stress modulate memory retention. Stress hormones critically implicated in this modulation are the glucocorticoids (corticosterone in rodents and cortisol in humans). Glucocorticoids can bind to two types of receptors: one with high affinity, the mineralcorticoid receptors and the other with low affinity, the glucocorticoid receptors (GRs). GRs are activated when the stress levels increases, like for example during an emotional experience.

We have investigated the hippocampal molecular mechanisms regulated downstream of glucocorticoid receptors (GRs) after a contextual inhibitory avoidance (IA) response in adult rats. We found that GRs are coupled to the activation of CaMKIIα, TrkB, ERK, Akt, PLCγ and CREB, as well as a significant induction of Arc and synaptic GluA1. Most of these changes, which are initiated by a non–genomic effect of glucocorticoid receptors, are also downstream of the activation of brain–derived neurotrophic factor (BDNF).
Hippocampal administration of BDNF, but not other neurotrophins, selectively rescues both the amnesia and the molecular impairments produced by glucocorticoid receptor inhibition.  We concluded that glucocorticoid receptors mediate long–term memory formation by recruiting the CaMKIIα–BDNF–CREB–dependent neural plasticity pathways.

We then investigated the same molecular cascade following an IA training evoked with a very strong shock, which leads to memory impairment. We will discuss these new data in the context of the GR-BDNF pathway.


Selected publications

Taubenfeld S.M., Riceberg J.S. New A., Alberini C.M. (2008) Preclinical assessment for selectively disrupting a traumatic memory via post-retrieval inhibition of glucocorticoid receptors. Biol Psychiatry. 65:249-57. Epub 2008 Aug 16.

Garcia-Osta A. and Alberini C.M. (2009) Amyloid beta mediates memory formation. Learning and Memory. 16:267-272.

Alberini C.M. (2009) Transcription Factors in Long-Term Memory and Synaptic Plasticity. Physiol Rev. 89:121-45.

Alberini C.M. (2009) Unwind: chronic stress exacerbates the deficits of Alzheimer's disease. Biol Psychiatry. 65:916-917.

Muravieva EV, Alberini CM. (2010) Limited efficacy of propranolol on the reconsolidation of fear memories. Learning and Memory 17:306-313. Print 2010 Jun.

Taubenfeld SM, Muravieva EV, Garcia-Osta A, Alberini CM. (2010) Disrupting the memory of places induced by drugs of abuse weakens motivational withdrawal in a context-dependent manner. Proc Natl Acad Sci U S A. 107:12345-12350. Epub 2010 Jun 21.Jun.

Chen DY, Stern SA, Garcia-Osta A, Saunier-Rebori B, Pollonini G, Bambah-Mukku D, Blitzer RD, Alberini CM. (2011) A critical role for IGF-II in memory consolidation and enhancement. Nature 469:491-497.

Alberini C.M. (2011). The role of reconsolidation and the dynamic process of long-term memory formation and storage. Frontiers in Behavioral Neuroscience, Volume 5, Article 12: 1-10.

Suzuki A, Stern SA, Bozdagi O, Huntley GW, Magistretti PJ, Alberini CM. (2011) Astrocyte-neuron lactate transport is required for long-term memory formation. Cell 144: 810-823.

Alberini CM, Chen DY (2012). Memory enhancement: consolidation, reconsolidation and insulin-like growth factor 2. Trends Neurosci. 35:274-83.

Chen DY, Bambah-Mukku D, Pollonini G, Alberini CM (2012). Glucocorticoid receptors recruit the CaMKIIα-BDNF-CREB pathways to mediate memory consolidation. Nat Neurosci. 15:1707-1714.

Scientific focus :

My laboratory studies the biological mechanisms of memory. In particular, we focus on the identification and characterization of the biological mechanisms that accompany long-term memory formation, storage and retrieval. Memory is a fundamental biological function and a critical component of our identity. Understanding the biological changes that underlie the formation and storage of long-term memory is important for developing strategies that change memory strength. Such knowledge may lead to therapeutic approaches for memory loss including those occurring in aging and Alzheimer's disease as well as for memory disorders due to pathogenically strong memories, such as those occurring in post-traumatic stress disorder (PTSD).

In order to become long-term memory, newly acquired information undergoes a number of changes that require the activation of cascades of gene expression. This is a universal feature of long-term memory processes, which, in fact, is found in several different forms of memory and is conserved throughout evolution. I am currently interested in 3 main questions: what are the nature and functions of the genes and proteins that, in different brain areas, play a critical role in long-term memory formation? How do these biological changes evolve over time? And, which are the biological mechanisms that accompany memory reorganization after retrieval? Stored memories can in fact become temporarily vulnerable if they are retrieved (reactivated). This phase of vulnerability after recall provides an opportunity for interventions that can either decrease or strengthen memories and prevent memory loss.

Memory Reconsolidation

Memory Reconsolidation  by Cristina M. Alberini

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After training in biology and immunology, I have now focused my interest on how the brain changes in response to external and internal stimuli. In particular, I am intrigued by how memories are formed, stored and elaborated. Memory is a fundamental biological function and a critical component of our identity. As such, it involves our brain, mind and psyche. I am interested in exploring the biological mechanisms of memory and their integration into complex behavioral manifestations. I am also interested in applying this knowledge in order to understand how memory becomes an integral part of pathologies such as addiction and trauma.