In:
Visual Neuroscience, Cambridge University Press (CUP), Vol. 19, No. 2 ( 2002-03), p. 175-185
Abstract:
Alpha-2 adrenoceptor agonists have previously been shown to
enhance neuronal survival in an optic nerve mechanical injury model and to protect photoreceptors in a light-induced degeneration
model. The purpose of this study was to examine the effect of the alpha-2 adrenoceptor agonist in a pressure-induced retinal
ischemia model. Brown-Norway rats were treated systemically or topically with alpha-2 adrenoceptor specific agonist
brimonidine. Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 50 min. The effect of
brimonidine on retinal ischemic injury was functionally assessed in the rats 7 d later using electroretinography (ERG).
Ischemia-induced retinal cell death was studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling
(TUNEL) staining. We found that brimonidine treatment significantly protected the retina from retinal ischemic injury in a dose-
and time-dependent manner. This protection can be achieved either by systemic or topical application and can be blocked by
pretreatment with the alpha-2 adrenoceptor antagonist, yohimbine. Using reverse transcription-polymerase chain reaction (RT-PCR)
and Western blot analysis, we found that brimonidine can up-regulate the expression of basic fibroblast growth factor,
bcl-2 and bcl-xl in the retina. The drug also can activate two major cell survival signaling pathways in the retina: the
extracellular-signal-regulated kinases (ERKs) and phosphatidylinositol-3′ kinase/protein kinase Akt pathways.
All these aforementioned factors may potentially contribute in mediating brimonidine's protective effect in this acute
retinal ischemia model.
Type of Medium:
Online Resource
ISSN:
0952-5238
,
1469-8714
DOI:
10.1017/S0952523802191152
Language:
English
Publisher:
Cambridge University Press (CUP)
Publication Date:
2002
detail.hit.zdb_id:
1489922-X
SSG:
12
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