The transient receptor potential (TRP) ion channels respond to a variety of stress-related stimuli in neurons. David Calkins, Ph.D., and colleagues recently demonstrated that mice missing the TRP vanilloid-1 subunit (TRPV1) had accelerated degeneration of retinal ganglion cells in response to elevated intraocular pressure – a critical risk factor in glaucoma.
Now, the researchers have explored how TRPV1 influences retinal ganglion cell survival in mouse models of glaucoma. They report in the Nov. 12 Journal of Neuroscience that exposure to elevated intraocular pressure increased expression of TRPV1 and its localization to excitatory synapses in retinal ganglion cells. They showed that this response was early and short-lived, and that TRPV1 had increased capacity to promote neuronal excitation and increase intracellular calcium.
The findings suggest that in response to a disease-related stressor, TRPV1 supports retinal neuron survival by transiently enhancing excitation at certain synapses. Understanding TRPV1’s pro-survival role could lead to new strategies for therapeutic intervention in glaucoma and other neurodegenerative conditions.
This research was supported the National Institutes of Health (grants EY017427, EY007135, GM007628), Research to Prevent Blindness, the BrightFocus Foundation and the Glaucoma Research Foundation.
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