Aerobic exercise is a common intervention for rehabilitation of motor, and more recently, cognitive function. While the underlying mechanisms are complex, BDNF may mediate much of the beneficial effects of exercise to these neurons. 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.
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Friday, April 04, 2014
Exercise protects retinas.
Gretchen Reynolds points to an article by Lawson et al. showing that the increase in blood levels of brain-derived neurotrophic factors (B.N.D.F.), known to promote neuron health and growth, apparently also raises BNDF levels in the retina. In a mouse model for retinal degeneration (vaguely analogous to human macular degeneration), exercise that raises BNDF levels inhibits the retinal deterioration caused by brief (4 hour) exposure to very bright lights.
Blog Categories:
aging,
brain plasticity,
exercise,
vision
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