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TrkB dimerization during development of the prefrontal cortex of the macaque
Author(s) -
Ohira Koji,
Shimizu Keiko,
Hayashi Motoharu
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1175
Subject(s) - tropomyosin receptor kinase b , prefrontal cortex , intracellular , tropomyosin receptor kinase c , tropomyosin receptor kinase a , brain derived neurotrophic factor , stimulation , chemistry , tyrosine kinase , biology , receptor , microbiology and biotechnology , neurotrophic factors , neuroscience , neurotrophin , biochemistry , growth factor , cognition , platelet derived growth factor receptor
To date, two subtypes of TrkB, a BDNF receptor, have been described. One is full‐length TrkB (TK+), which has a tyrosine kinase‐containing intracellular domain. The other is truncated TrkB (TK−), which has a short intracellular domain lacking the tyrosine kinase. In this study, we investigated the dimerization of TrkB subtypes in the developing monkey prefrontal cortex by means of cross‐linking. At embryonic day 120, the TK+/TK+ and the 100 kDa/100 kDa homodimers were observed with BDNF stimulation. At the newborn stage, the TK+/TK+ and the TK−/TK− homodimers were observed with BDNF stimulation. At the adult stage, the TK−/TK− homodimer and the TK+/TK− heterodimer were formed by BDNF stimulation. The levels of all dimers increased in proportion to the concentration of BDNF. Moreover, the dimers were clearly formed within 5 min of treatment with BDNF. BDNF and NT‐4/5 induced the dimers, whereas NT‐3 formed slight dimers but NGF did not. Furthermore, anti‐BDNF antibody inhibited the TrkB dimerization. Moreover, the intercellular binding proteins of TrkB were not cross‐linked by BS3. Therefore, these results suggest that the change in dimerization among TrkB subtypes occurs during development of the monkey prefrontal cortex. J. Neurosci. Res. 65:463–469, 2001. © 2001 Wiley‐Liss, Inc.