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Expression and role of sulfoglucuronyl (HNK-1) carbohydrate and its binding protein SBP-1 in developing rat cerebral cortex.

作者信息

Zhao Z, Nair S M, Chou D K, Tobet S A, Jungalwala F B

机构信息

Department of Biomedical Sciences, Eunice Kennedy Shriver Center for Mental Retardation, Waltham, Massachusetts 02452, USA.

出版信息

J Neurosci Res. 2000 Oct 15;62(2):186-205. doi: 10.1002/1097-4547(20001015)62:2<186::AID-JNR4>3.0.CO;2-C.

DOI:10.1002/1097-4547(20001015)62:2<186::AID-JNR4>3.0.CO;2-C
PMID:11020212
Abstract

Developmental expression of sulfoglucuronyl carbohydrate (SGC) and its binding protein, SBP-1 was studied in the rat cerebral cortex to understand their function. Between embryonic day (ED) 14-19, SBP-1 was strongly expressed in neurons of the ventricular zone and migrating neurons throughout the cortex. SBP-1 declined at birth and by postnatal day (PD) 3 only the latest arriving neurons in the most superficial segment of the cortical plate expressed SBP-1. Between ED 14-16, SGC was expressed in a thin row of glial cells near the ventricles and on their radial processes. Between ED 16-PD 3, SGC was not in neuronal cell soma, but was in neuronal plasma membranes and processes surrounding the neuronal perikarya. The expression of SGC declined similar to SBP-1 and both of them disappeared by PD 7. The expression of SBP-1 and SGC was chronologically coordinated with neuronal migration. SBP-1 was specifically expressed in immature neuronal nuclei and plasma membranes. SBP-1 and SGC were colocalized and were available for interaction with each other on neuronal cell membranes and processes. This was confirmed with isolated neurons in culture. As in vivo, the expression of SBP-1 in neurons declined with time in culture. The dissociated cortical neurons when plated on SBP-1 as a substratum produced extensive neuritic outgrowth. HNK-1, anti-SBP-1 antibodies and sulfoglucuronyl glycolipid, SGGL specifically and severely reduced neurite outgrowth. SBP-1-SGC interactions provide a potential mechanism for guidance and cell signaling, in the processes of neuronal migration and terminal differentiation.

摘要

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