MISC

2003年6月

Lack of Reelin causes malpositioning of nigral dopaminergic neurons: Evidence from comparison of normal and Reln(rl) mutant mice

JOURNAL OF COMPARATIVE NEUROLOGY
  • S Nishikawa
  • ,
  • S Goto
  • ,
  • K Yamada
  • ,
  • T Hamasaki
  • ,
  • Y Ushio

461
2
開始ページ
166
終了ページ
173
記述言語
英語
掲載種別
DOI
10.1002/cne.10610
出版者・発行元
WILEY-LISS

The reeler gene (Reln(rl), formerly rl) product Reelin controls neuronal migration and positioning and thereby plays a key role in brain development. Mutation of Reln leads to widespread disruption of laminar cortical regions and ectopia in some brainstem nuclei. In the embryonic striatum. of normal mice, a substantial expression of reelin mRNA has been documented; however, the anomalous positioning of neurons in the basal ganglia of reeler mice remains to be studied. We provide first evidence for a potential role of Reelin in the developmental formation of the substantia nigra. In reeler mutant mice lacking Reelin, dopaminergic neurons destined for the substantia nigra fail to migrate laterally and become anomalously clustered just lateral to the ventral tegmental area. Their axons appear to project to striatal patches forming "dopamine islands." Results from the normal mice show that, at the midembryonic stage, Reelin identified with CR-50 is highly concentrated in the ventral mesencephalon, where nigral dopaminergic neurons are in progress to migrate laterally to their eventual position of the adult brain. A combination of CR-50 labeling and anterograde axonal tracing provided evidence that embryonic striatal neurons may supply the ventral portion of the mesencephalon with Reelin through their axonal projections. We hypothesize that Reelin plays a role in the positioning of nigral dopaminergic neurons and that it can act as an environmental cue at a remote site far from its birthplace via a transaxonal delivery system.

Web of Science ® 被引用回数 : 44

リンク情報
DOI
https://doi.org/10.1002/cne.10610
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000182979400004&DestApp=WOS_CPL

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