PMID- 11006239
OWN - NLM
STAT- MEDLINE
DCOM- 20001012
LR  - 20220310
IS  - 0146-0404 (Print)
IS  - 0146-0404 (Linking)
VI  - 41
IP  - 11
DP  - 2000 Oct
TI  - Retrograde axonal transport of BDNF in retinal ganglion cells is blocked by acute 
      IOP elevation in rats.
PG  - 3460-6
AB  - PURPOSE: To determine whether acute experimental glaucoma in rats obstructs 
      retrograde transport of brain-derived neurotrophic factor (BDNF) to retinal 
      ganglion cells (RGCs). METHODS: Forty rats had unilateral injection of either 
      (125)I-BDNF (20 animals) or a mixture of (125)I-BDNF and 100-fold excess 
      nonradiolabeled BDNF (20 animals). In each group of 20 animals, eyes 
      contralateral to injection had either normal intraocular pressure (IOP; 10 
      animals) or IOP elevated to 25 mm Hg below the systolic blood pressure of the eye 
      (10 animals). In each group of 20 rats, ipsilateral eyes had IOP set at systolic 
      blood pressure (4 eyes), had optic nerve transection (10 eyes), or had normal IOP 
      (6 eyes). Six hours after injection, animals were killed and tissues were fixed, 
      embedded, and sectioned for autoradiography. Grain counts were performed over 
      retina and optic nerve using automated image analysis. RESULTS: IOP elevation to 
      25 mm Hg below systolic blood pressure (perfusion pressure [PP] 25) decreased 
      median retinal nerve fiber layer (NFL) grains by 38% compared with controls (P: < 
      0.001). Competition by cold BDNF reduced NFL grains by 28% (P: = 0.013). 
      Considering only the radioactivity representing specific retrograde transport of 
      BDNF, IOP elevation to PP25 reduced transport by 74%, whereas elevation to PP0 
      (equaling systolic blood pressure) reduced specific transport by 83%. 
      CONCLUSIONS: BDNF is transported retrogradely from the superior colliculus in 
      adult rats, and this transport is substantially inhibited by acute IOP elevation. 
      Deprivation of BDNF among RGCs may contribute to neuron loss in glaucoma.
FAU - Quigley, H A
AU  - Quigley HA
AD  - Glaucoma Research Laboratory, Wilmer Ophthalmological Institute, Johns Hopkins 
      University School of Medicine, Baltimore, Maryland, USA. hquigley@jhmi.edu
FAU - McKinnon, S J
AU  - McKinnon SJ
FAU - Zack, D J
AU  - Zack DJ
FAU - Pease, M E
AU  - Pease ME
FAU - Kerrigan-Baumrind, L A
AU  - Kerrigan-Baumrind LA
FAU - Kerrigan, D F
AU  - Kerrigan DF
FAU - Mitchell, R S
AU  - Mitchell RS
LA  - eng
GR  - EY 00361/EY/NEI NIH HHS/United States
GR  - EY 02120/EY/NEI NIH HHS/United States
GR  - EY 1765/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  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Autoradiography
MH  - *Axonal Transport
MH  - Blood Pressure
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Denervation
MH  - *Intraocular Pressure
MH  - Male
MH  - Nerve Fibers/*metabolism
MH  - Ocular Hypertension/*metabolism
MH  - Optic Disk/metabolism
MH  - Optic Nerve/physiology/surgery
MH  - Rats
MH  - Rats, Inbred BN
MH  - Retinal Ganglion Cells/*metabolism
MH  - Superior Colliculi/*metabolism
EDAT- 2000/09/28 11:00
MHDA- 2000/10/14 11:01
CRDT- 2000/09/28 11:00
PHST- 2000/09/28 11:00 [pubmed]
PHST- 2000/10/14 11:01 [medline]
PHST- 2000/09/28 11:00 [entrez]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3460-6.