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Nat Neurosci. 2017 Apr;20(4):529-539. doi: 10.1038/nn.4505. Epub 2017 Feb 13.

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

Author information

1
School of Biochemistry, University of Bristol, Bristol, UK.
2
Institute of Physiology, Academy of Sciences, Prague, Czech Republic.
3
Insitute of Medical Physiology, School of Medicine, University of Belgrade, Belgrade, Serbia.
4
Interdisciplinary Institute for Neuroscience, University of Bordeaux, Bordeaux, France.
5
Neuroscience Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, India.

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.

PMID:
28192396
DOI:
10.1038/nn.4505
[Indexed for MEDLINE]

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