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      • Record: found
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      Fragile X mental retardation protein and synaptic plasticity

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Loss of the translational repressor FMRP causes Fragile X syndrome. In healthy neurons, FMRP modulates the local translation of numerous synaptic proteins. Synthesis of these proteins is required for the maintenance and regulation of long-lasting changes in synaptic strength. In this role as a translational inhibitor, FMRP exerts profound effects on synaptic plasticity.

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          Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs.

          H. Markram, J Lübke, M Frotscher … (1997)
          Activity-driven modifications in synaptic connections between neurons in the neocortex may occur during development and learning. In dual whole-cell voltage recordings from pyramidal neurons, the coincidence of postsynaptic action potentials (APs) and unitary excitatory postsynaptic potentials (EPSPs) was found to induce changes in EPSPs. Their average amplitudes were differentially up- or down-regulated, depending on the precise timing of postsynaptic APs relative to EPSPs. These observations suggest that APs propagating back into dendrites serve to modify single active synaptic connections, depending on the pattern of electrical activity in the pre- and postsynaptic neurons.
          Article 0 comments Cited 843 times – based on 0 reviews     Review now
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            The molecular biology of memory storage: a dialogue between genes and synapses.

            E R Kandel (2001)
            One of the most remarkable aspects of an animal's behavior is the ability to modify that behavior by learning, an ability that reaches its highest form in human beings. For me, learning and memory have proven to be endlessly fascinating mental processes because they address one of the fundamental features of human activity: our ability to acquire new ideas from experience and to retain these ideas over time in memory. Moreover, unlike other mental processes such as thought, language, and consciousness, learning seemed from the outset to be readily accessible to cellular and molecular analysis. I, therefore, have been curious to know: What changes in the brain when we learn? And, once something is learned, how is that information retained in the brain? I have tried to address these questions through a reductionist approach that would allow me to investigate elementary forms of learning and memory at a cellular molecular level-as specific molecular activities within identified nerve cells.
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              Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type.

              Q Bi, G Bi, M Poo (1998)
              In cultures of dissociated rat hippocampal neurons, persistent potentiation and depression of glutamatergic synapses were induced by correlated spiking of presynaptic and postsynaptic neurons. The relative timing between the presynaptic and postsynaptic spiking determined the direction and the extent of synaptic changes. Repetitive postsynaptic spiking within a time window of 20 msec after presynaptic activation resulted in long-term potentiation (LTP), whereas postsynaptic spiking within a window of 20 msec before the repetitive presynaptic activation led to long-term depression (LTD). Significant LTP occurred only at synapses with relatively low initial strength, whereas the extent of LTD did not show obvious dependence on the initial synaptic strength. Both LTP and LTD depended on the activation of NMDA receptors and were absent in cases in which the postsynaptic neurons were GABAergic in nature. Blockade of L-type calcium channels with nimodipine abolished the induction of LTD and reduced the extent of LTP. These results underscore the importance of precise spike timing, synaptic strength, and postsynaptic cell type in the activity-induced modification of central synapses and suggest that Hebb's rule may need to incorporate a quantitative consideration of spike timing that reflects the narrow and asymmetric window for the induction of synaptic modification.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Brain
                Journal ID (iso-abbrev): Mol Brain
                Title: Molecular Brain
                Publisher: BioMed Central
                ISSN (Electronic): 1756-6606
                Publication date Collection: 2013
                Publication date (Electronic): 8 April 2013
                Volume: 6
                Page: 15
                Affiliations
                [1 ]The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA, 02139 46-3301, USA
                Article
                Publisher ID: 1756-6606-6-15
                DOI: 10.1186/1756-6606-6-15
                PMC ID: 3636002
                PubMed ID: 23566911
                SO-VID: 5299b0f1-8cce-4b14-bddb-16ac10bc6007
                Copyright © Copyright ©2013 Sidorov et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 9 January 2013
                Date accepted : 25 March 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Neurosciences
                Keywords: fmrp,fragile x,long-term depression,long-term potentiation,metabotropic glutamate receptor,protein synthesis,synaptic plasticity
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: fmrp, fragile x, long-term depression, long-term potentiation, metabotropic glutamate receptor, protein synthesis, synaptic plasticity

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