Publication
Aerobic Exercise Protects Retinal Function and Structure from Light-Induced Retinal Degeneration
Downloadable Content
- Persistent URL
- Last modified
- 02/20/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2014-02-12
- Publisher
- Society for Neuroscience
- Publication Version
- Copyright Statement
- © 2014 the authors
- Final Published Version (URL)
- Title of Journal or Parent Work
- ISSN
- 0270-6474
- Volume
- 34
- Issue
- 7
- Start Page
- 2406
- End Page
- 2412
- Grant/Funding Information
- This work was supported by National Institutes of Health Grants P30 EY006360 and NIH R01 EY014026-07S1 and the Abraham J. & Phyllis Katz Foundation (to J.H.B.), Rehabilitation Research and Development Service Veterans Affairs Research Career Scientist Award (to M.T.P.), Atlanta Veterans Administration Center of Excellence in Vision and Neurocognitive Rehabilitation, and Departmental Award from Research to Prevent Blindness.
- Abstract
- Aerobic exercise is a common intervention for rehabilitation of motor, and more recently, cognitive function (Intlekofer and Cotman, 2013; Wood et al., 2012). While the underlying mechanisms are complex, BDNF may mediate much of the beneficial effects of exercise to these neurons (Ploughman et al., 2007; Griffin et al., 2011; Real et al., 2013). We studied the effects of aerobic exercise on retinal neurons undergoing degeneration. We exercised wild-type BALB/c mice on a treadmill (10 m/min for 1 h) for 5 d/week or placed control mice on static treadmills. After 2 weeks of exercise, mice were exposed to either toxic bright light (10,000 lux) for 4 h to induce photoreceptor degeneration or maintenance dim light (25 lux). Bright light caused 75% loss of both retinal function and photoreceptor numbers. However, exercised mice exposed to bright light had 2 times greater retinal function and photoreceptor nuclei than inactive mice exposed to bright light. In addition, exercise increased retinal BDNF protein levels by 20% compared with inactive mice. Systemic injections of a BDNF tropomyosin-receptor-kinase (TrkB) receptor antagonist reduced retinal function and photoreceptor nuclei counts in exercised mice to inactive levels, effectively blocking the protective effects seen with aerobic exercise. The data suggest that aerobic exercise is neuroprotective for retinal degeneration and that this effect is mediated by BDNF signaling.
- Author Notes
- Keywords
- ALZHEIMERS-DISEASE
- retinal degeneration
- QUALITY-OF-LIFE
- RAT HIPPOCAMPUS
- ROD PHOTORECEPTORS
- PHYSICAL-ACTIVITY
- photoreceptors
- brain-derived neurotrophic factor
- NEUROTROPHIC FACTOR
- neuroprotection
- HIPPOCAMPAL FUNCTION
- Neurosciences & Neurology
- Neurosciences
- Science & Technology
- AXON REGENERATION
- treadmill
- NEUROSCIENCES
- PARKINSONS-DISEASE
- INJURED PERIPHERAL-NERVES
- Life Sciences & Biomedicine
- exercise
- Research Categories
- Health Sciences, Opthamology
- Health Sciences, General
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Publication File - rk58j.pdf | Primary Content | 2025-02-12 | Public | Download |