May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Glucagon–Related Peptides in the Mouse Retina and the Effects of Form Deprivation
Author Affiliations & Notes
  • F. Schaeffel
    Section Neurobiology of the Eye, Univ Eye Hospital Tubingen, Tubingen, Germany
  • U. Mathis
    Section Neurobiology of the Eye, Univ Eye Hospital Tubingen, Tubingen, Germany
  • Footnotes
    Commercial Relationships  F. Schaeffel, None; U. Mathis, None.
  • Footnotes
    Support  German Research Council Scha 518/11–1
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3336. doi:
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      F. Schaeffel, U. Mathis; Glucagon–Related Peptides in the Mouse Retina and the Effects of Form Deprivation . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3336.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: In chick retina, glucagon amacrine cells express the transcription factor ZENK in correlation with the sign of imposed defocus. In addition, pharmacological studies have shown that glucagon may act as a stop signal for axial eye growth. Even though glucagon could be a promising target to interfere with myopia development in chick, so far, it has not been detected immunohistochemically in the mammalian retina. The glucagon hormon family includes at least eight neuropeptides which are closely related in structure, distribution, function and receptors. We have studied their distribution in the mouse retina and whether they are regulated by visual experience. Methods: Black wildtype C57BL/6 mice were raised under a 12 hours light–dark cycle with light onset at 8:00 a.m. and were studied at postnatal ages p29–p36. Frosted hemispherical thin plastic shells served as eye diffusers. In all experiments the right eyes of mice wore plastic shells for various lengths of time, whereas the left eyes remained uncovered and served as controls. Transversal retinal cryostate sections were single or double labelled by indirect immunofluorescence for Egr–1 (the mammalian orthologue of ZENK), glucagon, glucagon–like peptide–2 (GLP–2), glucose dependent insulinotropic polypeptide (GIP), growth hormone releasing hormone (GHRH), pituitary adenylate cyclase–activating polypeptide (PACAP), secretin and vasoactive intestinal polypeptide (VIP). Results: (1) Glucagon itself was not detected in the mouse retina. (2) VIP, PACAP and GIP were identified by indirect immunofluorescence. VIP and PACAP displayed the expression pattern similar to the one described in the literature. GIP was localized for the first time in the mouse. (3) VIP was co–localized with Egr–1 which itself was strongly regulated by retinal illumination and even retinal image contrast. (4) Form deprivation imposed for various durations (1, 2, 6 and 24 h) had no effect on the expression of VIP, PACAP and GIP, at least at the protein level. (5) Similarly, even if the analysis was confined to cells that also expressed Egr–1, no difference was found between the VIP expression in form–deprived eyes and in eyes with normal vision. Conclusions: Several members of the glucagon super family are expressed in the mouse retina but their expression pattern does not seem to be regulated by visual experience.

Keywords: myopia • neuropeptides • retina: neurochemistry 

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