mGluR5-dependent modulation of dendritic excitability in CA1 pyramidal neurons mediated by enhancement of persistent Na+ currents

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Dendritic Na+ channels in pyramidal neurons are known to amplify synaptic signals, thereby facilitating action potential (AP) generation. However, the mechanisms that modulate dendritic Na+ channels have remained largely uncharacterized. Here, we report a new form of short-term plasticity in which proximal excitatory synaptic inputs to hippocampal CA1 pyramidal neurons transiently elevate dendritic excitability. High-frequency stimulations (HFS) to the Schaffer collateral (SC) pathway activate mGluR5-dependent Ca2+ signalling in the apical dendrites, which, with calmodulin, upregulates specifically Nav1.6 channel-mediated persistent Na+ currents (I-Na,I-P) in the dendrites. This HFS-induced increase in dendritic I-Na,I-P results in transient increases in the amplitude of excitatory postsynaptic potentials induced by both proximal SC and distal perforant path stimulation, leading to the enhanced probability of AP firing associated with decreased AP thresholds. Taken together, our study identifies dendritic I-Na,I-P as a novel target for mediating activity-dependent modulation of dendritic integration and neuronal output.
Publisher
WILEY
Issue Date
2018-09
Language
English
Article Type
Article
Keywords

METABOTROPIC GLUTAMATE RECEPTORS; BACKPROPAGATING ACTION-POTENTIALS; LONG-TERM POTENTIATION; SODIUM-CHANNELS; SYNAPTIC INTEGRATION; HIPPOCAMPAL-NEURONS; SENSORY NEURONS; I-H; ACTIVATION; PLASTICITY

Citation

JOURNAL OF PHYSIOLOGY-LONDON, v.596, no.17, pp.4141 - 4156

ISSN
0022-3751
DOI
10.1113/JP275999
URI
http://hdl.handle.net/10203/245907
Appears in Collection
BS-Journal Papers(저널논문)
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