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Metabotropic action of postsynaptic kainate receptors triggers hippocampal long-term potentiation

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)529–539
Number of pages11
JournalNature Neuroscience
Volume20
Issue number4
Early online date13 Feb 2017
DOIs
DateAccepted/In press - 13 Jan 2017
DateE-pub ahead of print - 13 Feb 2017
DatePublished (current) - Apr 2017

Abstract

Long-term potentiation (LTP) in the rat hippocampus is the most extensively studied cellular model for learning and memory. Induction of classical LTP involves an NMDA-receptor- and calcium-dependent increase in functional synaptic AMPA receptors, mediated by enhanced recycling of internalized AMPA receptors back to the postsynaptic membrane. Here we report a physiologically relevant NMDA-receptor-independent mechanism that drives increased AMPA receptor recycling and LTP. This pathway requires the metabotropic action of kainate receptors and activation of G protein, protein kinase C and phospholipase C. Like classical LTP, kainate-receptor-dependent LTP recruits recycling endosomes to spines, enhances synaptic recycling of AMPA receptors to increase their surface expression and elicits structural changes in spines, including increased growth and maturation. These data reveal a new and, to our knowledge, previously unsuspected role for postsynaptic kainate receptors in the induction of functional and structural plasticity in the hippocampus.

    Research areas

  • Hippocampus, Long-term potentiation, Membrane proteins

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  • Full-text PDF (accepted author manuscript)

    Rights statement: This is the author accepted manuscript (AAM). The final published version (version of record) is available online via Nature at http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.4505.html . Please refer to any applicable terms of use of the publisher.

    Accepted author manuscript, 23 MB, PDF-document

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