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How the brain adjusts to an increasing number of objects to remember?| old_uid | 11345 |
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| title | How the brain adjusts to an increasing number of objects to remember? |
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| start_date | 2012/05/04 |
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| schedule | 11h30 |
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| online | no |
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| location_info | salle de conférence Magendie |
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| details | Une invitation de Pauline Lafenêtre de NutriNeuro. |
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| summary | How much information can we remember for a short time interval? This is a question that has been discussed for many years. In the 1956, George A. Miller was perhaps the first to suggest that humans are only able to hold seven, plus or minus two digits, of information in a short retention time interval; this limit is generally called memory span. In our lab we are investigating how the brain copes to an increasing number of objects. To this aim, we developed a behavioral procedure to study object memory load in mice, and showed that mice, similarly to humans and primates, have a limited object memory span that is impaired by hippocampus damage. We then demonstrated that GluR1 AMPA-R phosphorylation increased within the hippocampus immediately after the exposure to high memory load but not to low memory load, suggesting that GluR1 AMPA-R phosphorylation confers plasticity and supports memory maintenance. This process is controlled by the activation of the N-Methyl-D-Aspartate (NMDA)-calcium-calmodulin-dependent-kinases (CaMK) II-protein-kinase A (PKA) pathways. The activation of the same pathways also controls long-term memory formation in high memory load condition, by promoting new protein synthesis. This suggests that the NMDA-CaMKII-PKA pathways exert a bidirectional control over both short and long term memory, by activating AMPA receptor phosphorylation and new protein synthesis, respectively. These results have important heuristic and clinical implications as they open new perspectives on the understanding of the role of the hippocampus in item memory, the molecular mechanisms underlying the regulation of short-term memory and its relationship with long term memory in high memory load conditions. This work was supported by a grant from Alzheimer's Association -NIRG-10-173992 to EDL. |
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| responsibles | Deris |
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