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      Expression of NMDA receptor-dependent LTP in the hippocampus: bridging the divide

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      Author(s): 1 , 3 , , 2 , 3 ,
      Publication date (Electronic):
      Journal: Molecular Brain
      Publisher: BioMed Central

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          Abstract

          A consensus has famously yet to emerge on the locus and mechanisms underlying the expression of the canonical NMDA receptor-dependent form of LTP. An objective assessment of the evidence leads us to conclude that both presynaptic and postsynaptic expression mechanisms contribute to this type of synaptic plasticity.

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          Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.

          Y Hayashi, S. Shi, J. Esteban … (2000)
          To elucidate mechanisms that control and execute activity-dependent synaptic plasticity, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPA-Rs) with an electrophysiological tag were expressed in rat hippocampal neurons. Long-term potentiation (LTP) or increased activity of the calcium/calmodulin-dependent protein kinase II (CaMKII) induced delivery of tagged AMPA-Rs into synapses. This effect was not diminished by mutating the CaMKII phosphorylation site on the GluR1 AMPA-R subunit, but was blocked by mutating a predicted PDZ domain interaction site. These results show that LTP and CaMKII activity drive AMPA-Rs to synapses by a mechanism that requires the association between GluR1 and a PDZ domain protein.
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            Synaptic AMPA receptor plasticity and behavior.

            Helmut Kessels, Roberto Malinow (2009)
            The ability to change behavior likely depends on the selective strengthening and weakening of brain synapses. The cellular models of synaptic plasticity, long-term potentiation (LTP) and depression (LTD) of synaptic strength, can be expressed by the synaptic insertion or removal of AMPA receptors (AMPARs), respectively. We here present an overview of studies that have used animal models to show that such AMPAR trafficking underlies several experience-driven phenomena-from neuronal circuit formation to the modification of behavior. We argue that monitoring and manipulating synaptic AMPAR trafficking represents an attractive means to study cognitive function and dysfunction in animal models.
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              Storage of spatial information by the maintenance mechanism of LTP.

              Eva Pastalkova, Peter Serrano, Deana Pinkhasova … (2006)
              Analogous to learning and memory storage, long-term potentiation (LTP) is divided into induction and maintenance phases. Testing the hypothesis that the mechanism of LTP maintenance stores information requires reversing this mechanism in vivo and finding out whether long-term stored information is lost. This was not previously possible. Recently however, persistent phosphorylation by the atypical protein kinase C isoform, protein kinase Mzeta (PKMz), has been found to maintain late LTP in hippocampal slices. Here we show that a cell-permeable PKMz inhibitor, injected in the rat hippocampus, both reverses LTP maintenance in vivo and produces persistent loss of 1-day-old spatial information. Thus, the mechanism maintaining LTP sustains spatial memory.
              Article 0 comments Cited 215 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Tim VP Bliss
                Graham L Collingridge
                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): 22 January 2013
                Volume: 6
                Page: 5
                Affiliations
                [1 ]Division of Neurophysiology, National Institute for Medical Research, Mill Hill, London NW7 1AA, UK
                [2 ]Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK
                [3 ]Department of Brain & Cognitive Sciences, College of Natural Sciences, Seoul National University, Rm 330, Bldg. 501 Shilim, Gwanak, Seoul, 151-746, Korea
                Article
                Publisher ID: 1756-6606-6-5
                DOI: 10.1186/1756-6606-6-5
                PMC ID: 3562207
                PubMed ID: 23339575
                SO-VID: f9ca13b6-91c3-43cd-a411-54959526bfc8
                Copyright © Copyright ©2013 Bliss and Collingridge; 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 : 8 January 2011
                Date accepted : 27 December 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Neurosciences
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                ScienceOpen disciplines: Neurosciences

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