Document Detail


Corpus callosum deficiency in transgenic mice expressing a truncated ephrin-A receptor.
MedLine Citation:
PMID:  14645492     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The A-class of the erythropoietin-producing hepatocellular carcinoma cell-derived (EphA) tyrosine kinase receptors and their ligands, the A-ephrins, play critical roles in the specification of topographic axon projection maps during development. In this study, the role of the EphA subfamily in callosal projections was investigated using transgenic mice expressing a kinase deletion mutant of EphA5. In approximately half of these transgenic mice, cerebral cortical neurons in various cortical regions (primary and secondary somatosensory cortices and frontal as well as visual areas) failed to project to the contralateral cortex. When commissural axons were examined with DiI labeling, few callosal fibers were found to traverse the midline in both the adult and neonatal transgenic mice. This defect in callosal development correlates with the expression of the transgene, because neurons in the superficial layers of the motor cortex, where transgene expression is low, show normal contralateral projection through the corpus callosum. In addition, multiple EphA receptors are expressed in callosal neurons and ephrin-A5 stimulates neurite outgrowth of callosal neurons in vitro. The midline glia structures important for callosal axon midline crossing appear normal in the transgenic mice, suggesting that the defects are unrelated to defective guidance structures at the midline. These observations suggest critical functions for EphA receptor in establishing callosal connections during brain development.
Authors:
Zhaoliang Hu; Xin Yue; Guanfang Shi; Yong Yue; David P Crockett; Jan Blair-Flynn; Kenneth Reuhl; Lino Tessarollo; Renping Zhou
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  23     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-12-03     Completed Date:  2003-12-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10963-70     Citation Subset:  IM    
Affiliation:
Laboratory for Cancer Research, College of Pharmacy, Rutgers University, Piscataway, New Jersey 08854, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Axons / pathology
Cerebral Cortex / pathology
Corpus Callosum / abnormalities*,  pathology
Gene Expression
In Situ Hybridization
Mice
Mice, Inbred Strains
Mice, Transgenic
Nervous System Malformations / genetics*,  pathology
Neurites / pathology
Neurons / pathology
RNA, Messenger / metabolism
Receptors, Eph Family / biosynthesis*,  genetics*
Transgenes
Chemical
Reg. No./Substance:
0/RNA, Messenger; EC 2.7.10.1/Receptors, Eph Family

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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