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Proc Natl Acad Sci U S A. 2018 Dec 18;115(51):13099-13104. doi: 10.1073/pnas.1808137115. Epub 2018 Nov 29.

Removal of clock gene Bmal1 from the retina affects retinal development and accelerates cone photoreceptor degeneration during aging.

Author information

1
Neuroscience Institute, Department of Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, GA 30310-1495.
2
Department of Pharmacy, University of Pisa, Pisa 56121, Italy.
3
Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA 30322-1013.
4
Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
5
Institute of Ophthalmology, Central South University, Changsha, Hunan 410008, China.
6
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294.
7
Neuroscience Institute, Department of Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, GA 30310-1495; miuvone@emory.edu gtosini@msm.edu.
8
Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA 30322-1013; miuvone@emory.edu gtosini@msm.edu.
9
Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322.

Abstract

The mammalian retina contains an autonomous circadian clock system that controls many physiological functions within this tissue. Previous studies on young mice have reported that removal of the key circadian clock gene Bmal1 from the retina affects the circadian regulation of visual function, but does not affect photoreceptor viability. Because dysfunction in the circadian system is known to affect cell viability during aging in other systems, we compared the effect of Bmal1 removal from the retina on visual function, inner retinal structure, and photoreceptor viability in young (1 to 3 months) and aged (24 to 26 months) mice. We found that removal of Bmal1 from the retina significantly affects visual information processing in both rod and cone pathways, reduces the thickness of inner retinal nuclear and plexiform layers, accelerates the decline of visual functions during aging, and reduces the viability of cone photoreceptors. Our results thus suggest that circadian clock dysfunction, caused by genetic or other means, may contribute to the decline of visual function during development and aging.

KEYWORDS:

aging; circadian rhythm; cone photoreceptor; development; retina

PMID:
30498030
PMCID:
PMC6305005
[Available on 2019-06-18]
DOI:
10.1073/pnas.1808137115
[Indexed for MEDLINE]

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