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Published in: Neurotoxicity Research 1/2012

01-01-2012

Mice Deficient in Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) are More Susceptible to Retinal Ischemic Injury In Vivo

Authors: K. Szabadfi, T. Atlasz, P. Kiss, B. Danyadi, A. Tamas, Zs. Helyes, H. Hashimoto, N. Shintani, A. Baba, G. Toth, R. Gabriel, D. Reglodi

Published in: Neurotoxicity Research | Issue 1/2012

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Abstract

Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuroprotective peptide exerting protective effects in neuronal injuries. We have provided evidence that PACAP is neuroprotective in several models of retinal degeneration in vivo. Our previous studies showed that PACAP treatment ameliorated the damaging effects of chronic hypoperfusion modeled by permanent bilateral carotid artery occlusion. We have also demonstrated in earlier studies that treatment with PACAP antagonists further aggravates retinal lesions. It has been shown that PACAP deficient mice have larger infarct size in cerebral ischemia. The aim of this 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 bilateral carotid artery occlusion followed by 2-week reperfusion period. 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, the morphometric analysis of the individual retinal layers, and the cell numbers in the inner nuclear and ganglion cell layers. Exogenous PACAP administration could partially protect against retinal degeneration in PACAP deficient mice. These results clearly show that endogenous PACAP reacts as a stress-response peptide that is necessary for endogenous protection against different retinal insults.
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Metadata
Title
Mice Deficient in Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) are More Susceptible to Retinal Ischemic Injury In Vivo
Authors
K. Szabadfi
T. Atlasz
P. Kiss
B. Danyadi
A. Tamas
Zs. Helyes
H. Hashimoto
N. Shintani
A. Baba
G. Toth
R. Gabriel
D. Reglodi
Publication date
01-01-2012
Publisher
Springer-Verlag
Published in
Neurotoxicity Research / Issue 1/2012
Print ISSN: 1029-8428
Electronic ISSN: 1476-3524
DOI
https://doi.org/10.1007/s12640-011-9254-y

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