To date, two subtypes of TrkB, a BDNF receptor, have been described. One is
full-length TrkB (TK+), which has a tyrosine kinase-containing intracellul
ar domain. The other is truncated TrkB (TK-), which has a short intracellul
ar domain lacking the tyrosine kinase. In this study, we investigated the d
imerization of TrkB subtypes in the developing monkey prefrontal cortex by
means of crosslinking. At embryonic day 120, the TK+/TK+ and the 100 kDa/10
0 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 wer
e formed by BDNF stimulation. The levels of all dimers increased in proport
ion 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, wh
ereas NT-3 formed slight dimers but NGF did not. Furthermore, anti-BDNF ant
ibody inhibited the TrkB dimerization. Moreover, the intercellular binding
proteins of TrkB were not cross-linked by BS3. Therefore, these results sug
gest that the change in dimerization among TrkB subtypes occurs during deve
lopment of the monkey prefrontal cortex. (C) 2001 Witey-Liss, Inc.