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by Leigh MacMillan | Posted on Friday, Mar. 14, 2014 — 8:00 AM
Understanding how neurons respond to stressors in degenerative disease could lead to the identification of new molecular targets for therapeutic intervention. The TRP (transient receptor potential) ion channels are candidates for mediating stress signals.
David Calkins, Ph.D., professor of Ophthalmology and Visual Sciences, and colleagues previously implicated the TRP vanilloid-1 subunit (TRPV1) in the stress response of retinal neurons (retinal ganglion cells, RGC) to elevated intraocular pressure (IOP) associated with glaucoma. They have now discovered that mice missing TRPV1 have accelerated neurodegeneration in response to elevated IOP. Mice missing TRPV1 had more severe deficits in axonal transport, degeneration of axons in the optic nerve and ganglion cell loss compared to control mice. The researchers also found that RGC from mice missing TRPV1 could not increase firing rate, and that pharmacological antagonism of TRPV1 accelerated RGC axon degeneration.
The findings, reported in the Feb. 26 Journal of Neuroscience, suggest that TRPV1 may help neurons survive stressors by boosting activity necessary for axonal signaling.
This research was supported by grants and awards from the National Institutes of Health (EY017427, EY007135), Research to Prevent Blindness and the Melza M. and Frank Theodore Barr Foundation through the Glaucoma Research Foundation.
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Health and Medicine, Reporter, Research Aliquots, David Calkins, glaucoma, Journal of Neuroscience, NEI, neurodegeneration, NIH, Ophthalmology and Visual Sciences, Reporter March 14 2014, Research to Prevent Blindness, retinal degeneration, Vanderbilt Eye Institute
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