PMID- 11948805
OWN - NLM
STAT- MEDLINE
DCOM- 20020530
LR  - 20191105
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 38
IP  - 2
DP  - 2002 Apr 15
TI  - Expression of glial fibrillary acidic protein and glutamine synthetase by Muller 
      cells after optic nerve damage and intravitreal application of brain-derived 
      neurotrophic factor.
PG  - 115-25
AB  - Muller glia play an important role in maintaining retinal homeostasis, and 
      brain-derived neurotrophic factor (BDNF) has proven to be an effective retinal 
      ganglion cell (RGC) neuroprotectant following optic nerve injury. The goal of 
      these studies was to investigate the relation between optic nerve injury and 
      Muller cell activation, and to determine the extent to which BDNF affects the 
      injury response of Muller cells. Using immunocytochemistry and Western blot 
      analysis, temporal changes in the expression of glial fibrillary acidic protein 
      (GFAP) and glutamine synthetase (GS) were examined in rats after optic nerve 
      crush alone, or in conjunction with an intravitreal injection of BDNF (5 microg). 
      GFAP protein levels were normal at 1 day post-crush, but increased approximately 
      9-fold by day 3 and remained elevated over the 2-week period studied. Muller cell 
      GS expression remained stable after optic nerve crush, but the protein showed a 
      transient shift in its cellular distribution; during the initial 24-h period 
      post-crush the GS protein appeared to translocate from the cell body to the inner 
      and outer glial processes, and particularly to the basal endfeet located in the 
      ganglion cell layer. BDNF alone, or in combination with optic nerve crush, did 
      not have a significant effect on the expression of either GFAP or GS compared 
      with the normal retina, or after optic nerve crush alone, respectively. The data 
      indicate that although BDNF is a potent neuroprotectant in the vertebrate retina, 
      it does not appear to have a significant influence on Muller cell expression of 
      either GS or GFAP in response to optic nerve injury.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Chen, Hao
AU  - Chen H
AD  - Department of Pharmacology, University of Tennessee at Memphis, USA.
FAU - Weber, Arthur J
AU  - Weber AJ
LA  - eng
GR  - EY11159/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  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Neuroprotective Agents)
RN  - EC 6.3.1.2 (Glutamate-Ammonia Ligase)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Glial Fibrillary Acidic Protein/analysis/*biosynthesis
MH  - Glutamate-Ammonia Ligase/analysis/*biosynthesis
MH  - Immunohistochemistry
MH  - Nerve Crush
MH  - Neuroglia/chemistry/*metabolism
MH  - Neuroprotective Agents/pharmacology
MH  - Optic Nerve Injuries/drug therapy/*metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Retinal Degeneration/drug therapy/metabolism/pathology
MH  - Retinal Ganglion Cells/pathology
EDAT- 2002/04/12 10:00
MHDA- 2002/05/31 10:01
CRDT- 2002/04/12 10:00
PHST- 2002/04/12 10:00 [pubmed]
PHST- 2002/05/31 10:01 [medline]
PHST- 2002/04/12 10:00 [entrez]
AID - 10.1002/glia.10061 [pii]
AID - 10.1002/glia.10061 [doi]
PST - ppublish
SO  - Glia. 2002 Apr 15;38(2):115-25. doi: 10.1002/glia.10061.