Short-term increases in transient receptor potential vanilloid-1 mediate stress-induced enhancement of neuronal excitation.

ABSTRACT: Progression of neurodegeneration in disease and injury is influenced by the response of individual neurons to stressful stimuli and whether this response includes mechanisms to counter declining function. Transient receptor potential (TRP) cation channels transduce a variety of disease-relevant stimuli and can mediate diverse stress-dependent changes in physiology, both presynaptic and postsynaptic. Recently, we demonstrated that knock-out or pharmacological inhibition of the TRP vanilloid-1 (TRPV1) capsaicin-sensitive subunit accelerates degeneration of retinal ganglion cell neurons and their axons with elevated ocular pressure, the critical stressor in the most common optic neuropathy, glaucoma. Here we probed the mechanism of the influence of TRPV1 on ganglion cell survival in mouse mod

SUBMITTER: Weitlauf C 

PROVIDER: S-EPMC4228139 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature