PMID- 10516311
OWN - NLM
STAT- MEDLINE
DCOM- 19991028
LR  - 20220310
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 20
DP  - 1999 Oct 15
TI  - Role of neurotrophin receptor TrkB in the maturation of rod photoreceptors and 
      establishment of synaptic transmission to the inner retina.
PG  - 8919-30
AB  - Brain-derived neurotrophic factor (BDNF) acts through TrkB, a receptor with 
      kinase activity, and mitigates light-induced apoptosis in adult mouse rod 
      photoreceptors. To determine whether TrkB signaling is necessary for rod 
      development and function, we examined the retinas of mice lacking all isoforms of 
      the TrkB receptor. Rod migration and differentiation occur in the mutant retina, 
      but proceed at slower rates than in wild-type mice. In postnatal day 16 (P16) 
      mutants, rod outer segment dimensions and rhodopsin content are comparable with 
      those of photoreceptors in P12 wild type (WT). Quantitative analyses of the 
      photoreceptor component in the electroretinogram (ERG) indicate that the gain and 
      kinetics of the rod phototransduction signal in dark-adapted P16 mutant and P12 
      WT retinas are similar. In contrast to P12 WT, however, the ERG in mutant mice 
      entirely lacks a b-wave, indicating a failure of signal transmission in the 
      retinal rod pathway. In the inner retina of mutant mice, although cells appear 
      anatomically and immunohistochemically normal, they fail to respond to prolonged 
      stroboscopic illumination with the normal expression of c-fos. Absence of the 
      b-wave and failure of c-fos expression, in view of anatomically normal inner 
      retinal cells, suggest that lack of TrkB signaling causes a defect in synaptic 
      signaling between rods and inner retinal cells. Retinal pigment epithelial cells 
      and cells in the inner retina, including Muller, amacrine, and retinal ganglion 
      cells, express the TrkB receptor, but rod photoreceptors do not. Moreover, inner 
      retinal cells respond to exogenous BDNF with c-fos expression and extracellular 
      signal-regulated kinase phosphorylation. Thus, interactions of rods with 
      TrkB-expressing cells must be required for normal rod development.
FAU - Rohrer, B
AU  - Rohrer B
AD  - Howard Hughes Medical Institute, School of Medicine, University of California San 
      Francisco, San Francisco, California 94143, USA.
FAU - Korenbrot, J I
AU  - Korenbrot JI
FAU - LaVail, M M
AU  - LaVail MM
FAU - Reichardt, L F
AU  - Reichardt LF
FAU - Xu, B
AU  - Xu B
LA  - eng
GR  - EY01919/EY/NEI NIH HHS/United States
GR  - EY11349/EY/NEI NIH HHS/United States
GR  - P50 MH048200-080005/MH/NIMH NIH HHS/United States
GR  - EY02162/EY/NEI NIH HHS/United States
GR  - R01 EY011349/EY/NEI NIH HHS/United States
GR  - R01 EY001919/EY/NEI NIH HHS/United States
GR  - P30 EY002162/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 9009-81-8 (Rhodopsin)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
EIN - J Neurosci 2000 Mar 1;20(5):2072
MH  - Aging/*physiology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Electroretinography
MH  - Immunohistochemistry
MH  - Light
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Mice, Knockout/genetics
MH  - Mutation/physiology
MH  - Proto-Oncogene Proteins c-fos/metabolism
MH  - Receptor, trkB/genetics/*physiology
MH  - Reference Values
MH  - Retina/cytology/drug effects/*physiology/radiation effects
MH  - Retinal Rod Photoreceptor Cells/*growth & development
MH  - Rhodopsin/metabolism
MH  - Synaptic Transmission/*physiology
PMC - PMC2757409
MID - NIHMS111501
EDAT- 1999/10/12 00:00
MHDA- 2000/03/25 00:00
PMCR- 2000/04/15
CRDT- 1999/10/12 00:00
PHST- 1999/10/12 00:00 [pubmed]
PHST- 2000/03/25 00:00 [medline]
PHST- 1999/10/12 00:00 [entrez]
PHST- 2000/04/15 00:00 [pmc-release]
AID - 3530 [pii]
AID - 10.1523/JNEUROSCI.19-20-08919.1999 [doi]
PST - ppublish
SO  - J Neurosci. 1999 Oct 15;19(20):8919-30. doi: 10.1523/JNEUROSCI.19-20-08919.1999.