Metabotropic action of postsynaptic kainate receptors triggers hippocampal long-term potentiation
Nat Neurosci. 2017-02-13; 20(4): 529-539
DOI: 10.1038/nn.4505
Lire sur PubMed
1. 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.
Petrovic MM(1)(2)(3), Viana da Silva S(4), Clement JP(5), Vyklicky L(2), Mulle
C(4), González-González IM(1), Henley JM(1).
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.
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.
DOI: 10.1038/nn.4505
PMID: 28192396 [Indexed for MEDLINE]