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Roles of mGluR5 in synaptic function and plasticity of the mouse thalamocortical pathway
Author(s) -
She WeiChi,
Quairiaux Charles,
Albright Michael J.,
Wang YuChi,
Sanchez Denisse E.,
Chang PohShing,
Welker Egbert,
Lu HuiChen
Publication year - 2009
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2009.06696.x
Subject(s) - neuroscience , barrel cortex , metabotropic glutamate receptor 5 , ampa receptor , synaptic plasticity , metabotropic glutamate receptor , dendritic spine , synapse , excitatory postsynaptic potential , glutamate receptor , biology , synaptic scaling , metaplasticity , sensory system , receptor , hippocampal formation , inhibitory postsynaptic potential , biochemistry
The group I metabotropic glutamate receptor 5 (mGluR5) has been implicated in the development of cortical sensory maps. However, its precise roles in the synaptic function and plasticity of thalamocortical (TC) connections remain unknown. Here we first show that in mGluR5 knockout (KO) mice bred onto a C57BL6 background cytoarchitectonic differentiation into barrels is missing, but the representations for large whiskers are identifiable as clusters of TC afferents. The altered dendritic morphology of cortical layer IV spiny stellate neurons in mGluR5 KO mice implicates a role for mGluR5 in the dendritic morphogenesis of excitatory neurons. Next, in vivo single‐unit recordings of whisker‐evoked activity in mGluR5 KO adults demonstrated a preserved topographical organization of the whisker representation, but a significantly diminished temporal discrimination of center to surround whiskers in the responses of individual neurons. To evaluate synaptic function at TC synapses in mGluR5 KO mice, whole‐cell voltage‐clamp recording was conducted in acute TC brain slices prepared from postnatal day 4–11 mice. At mGluR5 KO TC synapses, N ‐methyl‐ d ‐aspartate (NMDA) currents decayed faster and synaptic strength was more easily reduced, but more difficult to strengthen by Hebbian‐type pairing protocols, despite a normal developmental increase in α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPAR)‐mediated currents and presynaptic function. We have therefore demonstrated that mGluR5 is required for synaptic function/plasticity at TC synapses as barrels are forming, and we propose that these functional alterations at the TC synapse are the basis of the abnormal anatomical and functional development of the somatosensory cortex in the mGluR5 KO mouse.