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Homer 1a enhances spike‐induced calcium influx via L‐type calcium channels in neocortex pyramidal cells
Author(s) -
Yamamoto Kenji,
Sakagami Yu,
Sugiura Shigeki,
Inokuchi Kaoru,
Shimohama Shun,
Kato Nobuo
Publication year - 2005
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.1460-9568.2005.04278.x
Subject(s) - metabotropic glutamate receptor , voltage dependent calcium channel , neocortex , chemistry , neuroscience , calcium , metabotropic receptor , t type calcium channel , calcium signaling , glutamate receptor , microbiology and biotechnology , synaptic plasticity , biophysics , biology , receptor , biochemistry , organic chemistry
The scaffold protein family Homer/Vesl serves to couple surface receptors or channels with endoplasmic calcium release channels. Homer 1a/Vesl‐1S is regarded as regulating such coupling in an activity‐dependent manner. The present calcium photometry and electrophysiological measurement revealed that Homer 1a up‐regulates voltage‐dependent calcium channels (VDCCs), depending on inositol‐1,4,5‐trisphosphate (IP 3 ) receptors (IP 3 Rs). In rat neocortex pyramidal cells, intracellular injection by diffusion from the patch pipette (referred to as ‘infusion’) of Homer 1a protein enhanced spike‐induced calcium increase, depending on both the protein concentration and spike frequency. Induction of this enhancement was disrupted by blockers of key molecules of the mGluR–IP 3 signalling pathway, including metabotropic glutamate receptors (mGluRs), phospholipase C and IP 3 Rs. However, infusion of IP 3 failed to mimic the effect of Homer 1a, suggesting requirement for a second Homer 1a‐mediated signalling as well as the mGluR–IP 3 signalling. In contrast to the induction, maintenance of this enhancement was independent of the mGluR–IP 3 signalling, taking the form of augmented calcium influx via L‐type VDCCs. Presumably due to the VDCC up‐regulation, threshold currents for calcium spikes were reduced. Given that Homer 1a induction is thought to down‐regulate neural excitability and hence somatic spike firing, this facilitation of calcium spikes concomitant with such attenuated firing may well have a critical impact on bi‐directional synaptic plasticity.