May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Maturation of Mouse Cholinergic Amacrine Cells during Postnatal Development is Visual–experience–dependent
Author Affiliations & Notes
  • Z. Yang
    Ophthalmology, Baylor College Medicine, Houston, TX
  • J. Zhang
    Ophthalmology, Baylor College Medicine, Houston, TX
  • S.M. Wu
    Ophthalmology, Baylor College Medicine, Houston, TX
  • Footnotes
    Commercial Relationships  Z. Yang, None; J. Zhang, None; S.M. Wu, None.
  • Footnotes
    Support  EY 04446, EY 02520, the Retina Research Foundation (Houston), and Research Prevent to Blindness, Inc
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 4269. doi:
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      Z. Yang, J. Zhang, S.M. Wu; Maturation of Mouse Cholinergic Amacrine Cells during Postnatal Development is Visual–experience–dependent . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4269.

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

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Abstract

Abstract: : Purpose: The objective of this study is to investigate the effect of light deprivation on maturation, dendritic ramification, and distribution of cholinergic cells during mouse retinal development. Methods:Immunocytochemical experiments were performed on the mouse retinas from the postnatal day 0 (P0) through P30. Control mice were maintained in a regular 12–hour light/dark cycle. Light–deprived mice were obtained by rearing the animals in total darkness. Cholinergic cells were labeled with antibodies against choline acetyltransferase (ChAT). Antibodies against recoverin, calbindine, PKC, tyrosine hydroxylase, glutamine synthase, and GFAP were used to label photoreceptor, horizontal cells, rod bipolar cells, dopaminergic cells, Müller and glial cells, respectively. Results: In the control group, ChAT amacrine cells were detected in the neuroblastic layer and the ganglion cell layer (GCL) at the birth. ChAT labeling in the outer retina was transiently observed at P7 and it disappeared before eye opening. By P5, two characteristic cholinergic bands were clearly identified in the inner plexiform layer. Their staining became continuously thicker and brighter. By eye opening at P12, the cholinergic neurons were mature–like. At P15, the regularity index of the cholinergic mosaic peaked to 4.1 for cells in the inner nuclear layer (INL) and dropped to 2.57 for cells in the GCL. After eye opening, the space between two cholinergic bands increased continuously, indicating that these cells underwent refinement during the later phase of development. At P30, the regularity index of the cholinergic mosaic reached to 3.69 for cells in the INL and 3.34 for cells in the GCL. In addition, these cells grew normally in the first two postnatal weeks of dark rearing. However, under light deprivation conditions for up to three–four weeks, the thickness of the inner retina became thinner. The mosaic of cholinergic network was interrupted. The number of cholinergic neurons dropped significantly. Furthermore, photoreceptors, horizontal cells, rod bipolar cells, and dopaminergic cells appeared normal and were not affected by the light deprivation. The processes of glial cells grown vertically across the entire retinal thickness were observed in the dark–rearing animals. Conclusions: Our results suggest that the cholinergic neuron developing before eye opening is independent of the lighting condition, whereas their development after eye opening is greatly impeded by light deprivation. This later phase of development may be a critical period for the maturation and synaptic wiring of cholinergic amacrine cells in the mammalian retina.

Keywords: amacrine cells • plasticity • retinal connections, networks, circuitry 
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