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Impaired parallel fiber-Purkinje cell synapse stabilization during cerebellar development of mutant mice lacking the glutamate receptor δ2 subunit (GluRd2)

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/51748

Title: Impaired parallel fiber-Purkinje cell synapse stabilization during cerebellar development of mutant mice lacking the glutamate receptor δ2 subunit (GluRd2)
Authors: Kurihara, H. Browse this author
Hashimoto, K. Browse this author
Kano, M. Browse this author
Takayama, C. Browse this author →KAKEN DB
Sakimura, K. Browse this author
Mishina, M. Browse this author
Inoue, Y. Browse this author →KAKEN DB
Watanabe, M. Browse this author →KAKEN DB
Issue Date: 15-Dec-1997
Publisher: Society for Neuroscience
Journal Title: The Journal of neuroscience : the official journal of the Society for Neuroscience
Volume: 17
Issue: 24
Start Page: 9613
End Page: 9623
Publisher DOI: 10.1523/JNEUROSCI.17-24-09613.1997
PMID: 09391016
Abstract: The glutamate receptor delta2 subunit (GluRdelta2) is specifically expressed in cerebellar Purkinje cells (PCs) from early developmental stages and is selectively localized at dendritic spines forming synapses with parallel fibers (PFs). Targeted disruption of the GluRdelta2 gene leads to a significant reduction of PF-->PC synapses. To address its role in the synaptogenesis, the morphology and electrophysiology of PF-->PC synapses were comparatively examined in developing GluRdelta2 mutant and wild-type cerebella. PCs in GluRdelta2 mutant mice were normally produced, migrated, and formed spines, as did those in wild-type mice. At the end of the first postnatal week, 74-78% of PC spines in both mice formed immature synapses, which were characterized by small synaptic contact, few synaptic vesicles, and incomplete surrounding by astroglial processes, eliciting little electrophysiological response. During the second and third postnatal weeks when spines and terminals are actively generated, the percentage of PC spines forming synapses attained 98-99% in wild type but remained as low as 55-60% in mutants, and the rest were unattached to any nerve terminals. As a result, the number of PF synapses per single-mutant PCs was reduced to nearly a half-level of wild-type PCs. Parallelly, PF stimulation less effectively elicited EPSCs in mutant PCs than in wild-type PCs during and after the second postnatal week. These results suggest that the GluRdelta2 is involved in the stabilization and strengthening of synaptic connectivity between PFs and PCs, leading to the association of all PC spines with PF terminals to form functionally mature synapses.
Relation: http://www.jneurosci.org/content/17/24/9613.full.pdf+html
Type: article
URI: http://hdl.handle.net/2115/51748
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 渡邉 雅彦

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