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Abstract
Pituitary adenylate cyclase activating polypeptide (PACAP) is a neurotrophic and neuroprotective
peptide. PACAP and its receptors are widely distributed in the retina. A number of
reports provided evidence that PACAP is neuroprotective in retinal degenerations.
The current study compared retina cell type-specific differences in young (3-4months)
and aged adults (14-16months), of wild-type (WT) mice and knock-out (KO) mice lacking
endogenous PACAP production during the course of aging. Histological, immunocytochemical
and Western blot examinations were performed. The staining for standard neurochemical
markers (tyrosine hydroxylase for dopaminergic cells, calbindin 28 kDa for horizontal
cells, protein kinase Cα for rod bipolar cells) of young adult PACAP KO retinas showed
no substantial alterations compared to young adult WT retinas, except for the specific
PACAP receptor (PAC1-R) staining. We could not detect PAC1-R immunoreactivity in bipolar
and horizontal cells in young adult PACAP KO animals. Some other age-related changes
were observed only in the PACAP KO mice only. These alterations included horizontal
and rod bipolar cell dendritic sprouting into the photoreceptor layer and decreased
ganglion cell number. Also, Müller glial cells showed elevated GFAP expression compared
to the aging WT retinas. Furthermore, Western blot analyses revealed significant differences
between the phosphorylation state of ERK1/2 and JNK in KO mice, indicating alterations
in the MAPK signaling pathway. These results support the conclusion that endogenous
PACAP contributes to protection against aging of the nervous system.