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Increased sensitivity of PACAP knockout mice to retinal ischemia
Author(s) -
Reglodi D.,
Szabadfi K.,
Kiss P.,
Tamas A.,
Hashimoto H.,
Baba A.,
Shintani N.,
Gabriel R.,
Helyes Z.,
Atlasz T.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.641.4
Subject(s) - retinal , neuroprotection , retina , knockout mouse , endogeny , ischemia , in vivo , endocrinology , medicine , retinal degeneration , electroretinography , biology , neuroscience , ophthalmology , receptor , microbiology and biotechnology
Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuroprotective peptide exerting protective effects in neuronal injuries. PACAP is protective in several models of retinal degeneration in vivo. Our previous studies have shown that PACAP treatment ameliorates the damaging effects of chronic hypoperfusion modeled by permanent bilateral carotid artery occlusion. The aim of the present study was to compare the degree of retinal damage in wild type and PACAP deficient mice in ischemic retinal insult. Mice underwent 10 min of carotid artery occlusion followed by 2‐week reperfusion. Retinas were then processed for histological analysis. It was found that PACAP deficient mice had significantly greater retinal damage, as shown by the thickness of the whole retina and the morphometric analysis of the individual retinal layers, such as inner and outer plexiform and inner and outer nuclear layers. The retinal damage in PACAP knockout animals could be attenuated by exogenous intravitreal PACAP. These results clearly show that endogenous PACAP reacts as a stress‐response peptide that is necessary for endogenous protection against different neuronal insults.