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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-9-29
pubmed:abstractText
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 (IP3) receptors (IP3Rs). 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-IP3 signalling pathway, including metabotropic glutamate receptors (mGluRs), phospholipase C and IP3Rs. However, infusion of IP3 failed to mimic the effect of Homer 1a, suggesting requirement for a second Homer 1a-mediated signalling as well as the mGluR-IP3 signalling. In contrast to the induction, maintenance of this enhancement was independent of the mGluR-IP3 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1338-48
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16190889-Animals, pubmed-meshheading:16190889-Calcium, pubmed-meshheading:16190889-Calcium Channels, L-Type, pubmed-meshheading:16190889-Calcium Signaling, pubmed-meshheading:16190889-Carrier Proteins, pubmed-meshheading:16190889-Electrophysiology, pubmed-meshheading:16190889-Electroshock, pubmed-meshheading:16190889-Male, pubmed-meshheading:16190889-Membrane Potentials, pubmed-meshheading:16190889-Neocortex, pubmed-meshheading:16190889-Patch-Clamp Techniques, pubmed-meshheading:16190889-Photometry, pubmed-meshheading:16190889-Pyramidal Cells, pubmed-meshheading:16190889-Rats, pubmed-meshheading:16190889-Rats, Wistar, pubmed-meshheading:16190889-Receptors, Metabotropic Glutamate, pubmed-meshheading:16190889-Recombinant Proteins, pubmed-meshheading:16190889-Seizures, pubmed-meshheading:16190889-Type C Phospholipases
pubmed:year
2005
pubmed:articleTitle
Homer 1a enhances spike-induced calcium influx via L-type calcium channels in neocortex pyramidal cells.
pubmed:affiliation
Department of Integrative Brain Science, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.
pubmed:publicationType
Journal Article