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Elevation of intraocular pressure in relation to retinal diseases
Author(s) -
VidalSanz M.,
ValienteSoriano F.J.,
Rovere G.,
NadalNicolás F.M.,
SalinasNavarro M.,
AgudoBarriuso M.,
VillegasPérez M.P.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.01364
Subject(s) - ophthalmology , glaucoma , intraocular pressure , population , medicine , neurotrophic factors , retinal , receptor , environmental health
Summary Intraocular pressure remains the only modifiable risk factor in glaucoma, a disease characterized by progressive loss or retinal ganglion cells ( RGC s) and visual field deficits leading to blindness. Using two rat models of chronic ( COH ) or acute ( AOH ) ocular hypertension we study the response of the general population of RGC s responsible for image‐forming visual information and the intrinsically photosensitive population of RGC s responsible for nonimage‐forming visual information, identified with Brn3a and melanopsin antibodies, respectively. For AOH the anterior chamber of the left eye was cannulated and connected to saline elevated 1½ meters for 75 minutes. COH was induced by laser‐photocoagulation of limbar tissues. In both models prior to OH a single intravitreal injection of brain derived neurotrophic factor (5 μ g BDNF in 1% albumin PBS ) or vehicle was administered. Re retinas were examined at 12 or 15 days after COH or 3, 7, 14, or 45 days after AOH to identify surviving Brn3a + RGC s and m + RGC s. COH induced comparable loss of RGC s but only Brn3a + RGC s responded to BDNF . After AOH , Brn3a + RGC s died progressively while m + RGC s did not, and BDNF induced a permanent protection up to 45 days after AOH in both types of RGC s.