Linked Life Data

11739579

Source:http://linkedlifedata.com/resource/pubmed/id/11739579

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2001-12-12
pubmed:abstractText
Climbing fiber (CF) synapse formation onto cerebellar Purkinje cells (PCs) is critically dependent on the synaptogenesis from parallel fibers (PFs), the other input to PCs. Previous studies revealed that deletion of the glutamate receptor delta2 subunit (GluRdelta2) gene results in persistent multiple CF innervation of PCs with impaired PF synaptogenesis, whereas mutation of the metabotropic glutamate receptor subtype 1 (mGluR1) gene causes multiple CF innervation with normal PF synaptogenesis. We demonstrate that atypical CF-mediated EPSCs (CF-EPSCs) with slow rise times and small amplitudes coexisted with typical CF-EPSCs with fast rise times and large amplitudes in PCs from GluRdelta2 mutant cerebellar slices. CF-EPSCs in mGluR1 mutant and wild-type PCs had fast rise times. Atypical slow CF responses of GluRdelta2 mutant PCs were associated with voltage-dependent Ca(2+) signals that were confined to PC distal dendrites. In the wild-type and mGluR1 mutant PCs, CF-induced Ca(2+) signals involved both proximal and distal dendrites. Morphologically, CFs of GluRdelta2 mutant mice extended to the superficial regions of the molecular layer, whereas those of wild-type and mGluR1 mutant mice did not innervate the superficial one-fifth of the molecular layer. It is therefore likely that surplus CFs of GluRdelta2 mutant mice form ectopic synapses onto distal dendrites, whereas those of wild-type and mGluR1 mutant mice innervate proximal dendrites. These findings suggest that GluRdelta2 is required for consolidating PF synapses and restricting CF synapses to the proximal dendrites, whereas the mGluR1-signaling pathway does not affect PF synaptogenesis but is involved in eliminating surplus CF synapses at the proximal dendrites.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9701-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11739579-Aging, pubmed-meshheading:11739579-Animals, pubmed-meshheading:11739579-Calcium Signaling, pubmed-meshheading:11739579-Cell Membrane, pubmed-meshheading:11739579-Cerebellum, pubmed-meshheading:11739579-Crosses, Genetic, pubmed-meshheading:11739579-Dendrites, pubmed-meshheading:11739579-Excitatory Postsynaptic Potentials, pubmed-meshheading:11739579-Mice, pubmed-meshheading:11739579-Mice, Inbred Strains, pubmed-meshheading:11739579-Mice, Mutant Strains, pubmed-meshheading:11739579-Mutation, pubmed-meshheading:11739579-Nerve Fibers, pubmed-meshheading:11739579-Olivary Nucleus, pubmed-meshheading:11739579-Patch-Clamp Techniques, pubmed-meshheading:11739579-Purkinje Cells, pubmed-meshheading:11739579-Reaction Time, pubmed-meshheading:11739579-Receptors, Glutamate, pubmed-meshheading:11739579-Receptors, Metabotropic Glutamate, pubmed-meshheading:11739579-Signal Transduction, pubmed-meshheading:11739579-Synapses
pubmed:year
2001
pubmed:articleTitle
Roles of glutamate receptor delta 2 subunit (GluRdelta 2) and metabotropic glutamate receptor subtype 1 (mGluR1) in climbing fiber synapse elimination during postnatal cerebellar development.
pubmed:affiliation
Department of Physiology, Kanazawa University School of Medicine, Takara-machi, Kanazawa 920-8640, Japan.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't