Journal
NEUROTOXICITY RESEARCH
Volume 21, Issue 1, Pages 41-48Publisher
SPRINGER
DOI: 10.1007/s12640-011-9254-y
Keywords
PACAP knockout; Retina; Transient ischemia; Endogenous PACAP; Intravitreal PACAP treatment
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Funding
- OTKA [K72592, CNK78480]
- Bolyai Scholarship
- Japan Society for the Promotion of Science
- Richter Gedeon Centenary Foundation [SROP-4.2.1.B-10/2/KONV-2010-0002]
- Funding Program for Next Generation World-Leading Researchers
- Momentum Program of the Hungarian Academy of Sciences [SROP 4.2.1.B-10/2/KONV-2010-0002]
- [F67830]
- [T73044]
- [ETT278-04/2009]
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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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