Linked Life Data

19778510

Source:http://linkedlifedata.com/resource/pubmed/id/19778510

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-9-25
pubmed:abstractText
Kainate receptors signal through both ionotropic and metabotropic pathways. The high-affinity subunits, GluK4 and GluK5, are unique among the five receptor subunits, as they do not form homomeric receptors but modify the properties of heteromeric assemblies. Disruption of the Grik4 gene locus resulted in a significant reduction in synaptic kainate receptor currents. Moreover, ablation of GluK4 and GluK5 caused complete loss of synaptic ionotropic kainate receptor function. The principal subunits were distributed away from postsynaptic densities and presynaptic active zones. There was also a profound alteration in the activation properties of the remaining kainate receptors. Despite this, kainate receptor-mediated inhibition of the slow afterhyperpolarization current (I(sAHP)), which is dependent on metabotropic pathways, was intact in GluK4/GluK5 knockout mice. These results uncover a previously unknown obligatory role for the high-affinity subunits for ionotropic kainate receptor function and further demonstrate that kainate receptor participation in metabotropic signaling pathways does not require their classic role as ion channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1097-4199
pubmed:author
pubmed:issnType
Electronic
pubmed:day
24
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
818-29
pubmed:dateRevised
2011-9-29
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
High-affinity kainate receptor subunits are necessary for ionotropic but not metabotropic signaling.
pubmed:affiliation
Department of Physiology, Northwestern University School of Medicine, 303 E Chicago Avenue, Chicago, IL 60611, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural