COMPARISON OF RPTP-ZETA BETA, PHOSPHACAN, AND TRKB MESSENGER-RNA EXPRESSION IN THE DEVELOPING AND ADULT-RAT NERVOUS-SYSTEM AND INDUCTION OFRPTP-ZETA/BETA AND PHOSPHACAN MESSENGER-RNA FOLLOWING BRAIN INJURY/

Citation
Se. Snyder et al., COMPARISON OF RPTP-ZETA BETA, PHOSPHACAN, AND TRKB MESSENGER-RNA EXPRESSION IN THE DEVELOPING AND ADULT-RAT NERVOUS-SYSTEM AND INDUCTION OFRPTP-ZETA/BETA AND PHOSPHACAN MESSENGER-RNA FOLLOWING BRAIN INJURY/, Molecular brain research, 40(1), 1996, pp. 79-96
Citations number
48
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
0169328X
Volume
40
Issue
1
Year of publication
1996
Pages
79 - 96
Database
ISI
SICI code
0169-328X(1996)40:1<79:CORBPA>2.0.ZU;2-8
Abstract
The receptor protein tyrosine phosphatase (RPTP)zeta/beta and a major isoform, phosphacan, a chondroitin sulfate proteoglycan that contains the RPTP zeta/beta extracellular domain but not the transmembrane and intracellular phosphatase domains, are expressed abundantly in the ner vous system, primarily by astroglia. Because of similarities in the ex pression patterns of RPTP zeta/beta and the receptor tyrosine kinase T rkB, we investigated whether RNAs encoding these proteins were co-loca lized during development, which would suggest that these molecules mig ht functionally interact in vivo. By in-situ hybridization, we noted e xtensive areas of overlap in the expression of trkB and RPTP zeta/beta mRNAs in the developing peripheral and central nervous systems. Analy sis with a probe specific for the catalytic TrkB isoform suggested tha t RPTP zeta/beta and non-catalytic trkB mRNAs were co-expressed in par ticular regions of the nervous system while the catalytic trkB and RPT P zeta/beta transcripts were also, but to a lesser extent. RPTP zeta/b eta and phosphacan expression were extremely similar, differing partic ularly in the level of expression in the ventricular and subventricula r zones, hippocampus, and ependyma. Furthermore, both RPTP zeta/beta a nd phosphacan mRNAs were found in several subsets of neurons as well a s astrocytes. Following CNS injury, we observed robust induction of RP TP zeta/beta mRNA in areas of axonal sprouting, and of both RPTP zeta/ beta and phosphacan mRNAs in areas of glial scarring, implying that th e encoded proteins and the cell adhesion molecules and extracellular m atrix proteins to which they bind may contribute to recovery from inju ry and perhaps regulation of axonal regrowth in the nervous system.