PMID- 16866620
OWN - NLM
STAT- MEDLINE
DCOM- 20060914
LR  - 20071114
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 23
IP  - 7
DP  - 2006 Jul
TI  - Traumatic brain injury induced neuroprotection of retinal ganglion cells to optic 
      nerve crush.
PG  - 1072-82
AB  - Optic nerve crush injury leads to death of retinal ganglion cells (RGCs), both as 
      a direct result of the primary injury and via secondary degeneration induced by 
      neurotoxins secreted by dying RGCs. Studies have shown that, if optic nerve crush 
      is preceded by an unrelated injury to another part of the central nervous system, 
      for example, the spinal cord, the ensuing T cell-mediated protective autoimmunity 
      results in a significant increase in RGC survival. In this study, we used the 
      controlled cortical impact paradigm to induce unilateral traumatic brain injury 
      (TBI) in rats at different times before they were contralaterally subjected to a 
      mild optic nerve crush. Survival of RGCs, assessed 2 weeks after crush injury, 
      was significantly increased when the crush was inflicted 11 days after TBI, but 
      not when the two injuries were concomitant. The beneficial effect was unaffected 
      by injection of low-dose methylprednisolone MP (1 mg/kg), but was inhibited after 
      a high-dose injection (30 mg/kg). Brain-derived neurotrophic factor (BDNF) mRNA, 
      assayed at intervals after TBI, was increased in the retina ipsilateral to TBI 
      but decreased in the contralateral retina. BDNF peaked 1 day after TBI, decreased 
      on day 11, and rose again on day 21. It thus seems that brain injury sustained a 
      certain time before optic nerve injury has a protective effect on RGC survival. 
      This neuroprotective effect, which appears unrelated to retinal BDNF, is 
      inhibited by high-dose MP, commonly used clinically to treat traumatic optic 
      neuropathy.
FAU - Ben Simon, Guy J
AU  - Ben Simon GJ
AD  - Jules Stein Eye Institute and Department of Ophthalmology, David Geffen School of 
      Medicine at UCLA, Los Angeles, California, USA. guybensimon@gmail.com
FAU - Hovda, David A
AU  - Hovda DA
FAU - Harris, Neil G
AU  - Harris NG
FAU - Gomez-Pinilla, Fernando
AU  - Gomez-Pinilla F
FAU - Goldberg, Robert A
AU  - Goldberg RA
LA  - eng
GR  - NS27544/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Brain Injuries/metabolism/*pathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Male
MH  - *Nerve Crush
MH  - Optic Nerve Injuries/metabolism/*pathology/*prevention & control
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Retinal Ganglion Cells/metabolism/*pathology
EDAT- 2006/07/27 09:00
MHDA- 2006/09/15 09:00
CRDT- 2006/07/27 09:00
PHST- 2006/07/27 09:00 [pubmed]
PHST- 2006/09/15 09:00 [medline]
PHST- 2006/07/27 09:00 [entrez]
AID - 10.1089/neu.2006.23.1072 [doi]
PST - ppublish
SO  - J Neurotrauma. 2006 Jul;23(7):1072-82. doi: 10.1089/neu.2006.23.1072.