PMID- 10716894
OWN - NLM
STAT- MEDLINE
DCOM- 20000418
LR  - 20091119
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 162
IP  - 1
DP  - 2000 Mar
TI  - Role for basic fibroblast growth factor (FGF-2) in tyrosine kinase (TrkB) 
      expression in the early development and innervation of the auditory receptor: in 
      vitro and in situ studies.
PG  - 121-45
AB  - A previous study showed that basic fibroblast growth factor (FGF-2) promotes the 
      effects of brain-derived neurotrophic factor (BDNF) on migration and neurite 
      outgrowth from the cochleovestibular ganglion (CVG). This suggests that FGF-2 may 
      up-regulate the receptor for BDNF. Thus we have examined TrkB expression during 
      CVG formation and otic innervation in vitro and in the chicken embryo using 
      immunohistochemistry. Following anatomical staging according to 
      Hamburger-Hamilton, results were compared with mRNA expression in vitro using in 
      situ hybridization. In the embryo at stage 16 (E2+) clusters of either lightly 
      stained or immunonegative cells occurred within the otocyst and among those 
      migrating to the CVG. By stage 22 (E3.5), immunostaining was concentrated in the 
      CVG perikarya and invaded the processes growing into the otic epithelium but not 
      into the rhombencephalon. Subsequently TrkB expression decreased in the perikarya 
      and became localized in the leading processes of the fibers invading the 
      epithelium and in the structures participating in synapse formation with the hair 
      cells. In vitro there was moderate immunostaining and modest in situ 
      hybridization for trkB in the neuroblasts migrating from the otocyst under 
      control conditions. In contrast, neuroblasts previously exposed to FGF-2 
      exhibited accelerated migration and differentiation, with increased trkB mRNA 
      expression. Morphological differentiation was associated with more intense 
      immunostaining of processes than cell bodies. Evidently TrkB shifts its 
      expression sequentially from sites engaged in migration, ganglion cell 
      differentiation, axonal outgrowth, epithelial innervation, and synapse formation. 
      FGF-2 may promote the role of BDNF in these developmental events by upregulating 
      the TrkB receptor.
CI  - Copyright 2000 Academic Press.
FAU - Brumwell, C L
AU  - Brumwell CL
AD  - Department of Anatomy, University of Connecticut Health Center, Farmington, 
      Connecticut, 06030-3405, USA.
FAU - Hossain, W A
AU  - Hossain WA
FAU - Morest, D K
AU  - Morest DK
FAU - Bernd, P
AU  - Bernd P
LA  - eng
GR  - R01NS29613/NS/NINDS NIH HHS/United States
GR  - T32DC00025/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (RNA, Messenger)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Antibody Specificity
MH  - Axons/physiology
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Cell Differentiation/drug effects/physiology
MH  - Cells, Cultured
MH  - Chick Embryo
MH  - Epithelium/innervation
MH  - Fibroblast Growth Factor 2/*pharmacology
MH  - Gene Expression Regulation, Developmental/*drug effects
MH  - In Situ Hybridization
MH  - Neurons, Afferent/chemistry/cytology/enzymology
MH  - RNA, Messenger/analysis
MH  - Receptor, trkB/analysis/*genetics/immunology
MH  - Spiral Ganglion/cytology/*embryology
MH  - Synapses/physiology
MH  - Vestibulocochlear Nerve/cytology/*embryology
EDAT- 2000/03/16 09:00
MHDA- 2000/04/25 09:00
CRDT- 2000/03/16 09:00
PHST- 2000/03/16 09:00 [pubmed]
PHST- 2000/04/25 09:00 [medline]
PHST- 2000/03/16 09:00 [entrez]
AID - S0014-4886(00)97317-5 [pii]
AID - 10.1006/exnr.2000.7317 [doi]
PST - ppublish
SO  - Exp Neurol. 2000 Mar;162(1):121-45. doi: 10.1006/exnr.2000.7317.