1. Role of TRPM2 cation channels in dorsal root ganglion of rats after experimental spinal cord injury.
- Author
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Naziroğlu M, Uğuz AC, Ismailoğlu Ö, Çiğ B, Özgül C, and Borcak M
- Subjects
- Action Potentials drug effects, Action Potentials physiology, Animals, Boron Compounds pharmacology, Calcium metabolism, Calcium Channels, L-Type metabolism, Cinnamates pharmacology, Disease Models, Animal, Ganglia, Spinal pathology, Hydrogen Peroxide pharmacology, Male, Neurons drug effects, Neurons physiology, Oxidants pharmacology, Patch-Clamp Techniques, Rats, Rats, Wistar, Statistics, Nonparametric, TRPM Cation Channels antagonists & inhibitors, ortho-Aminobenzoates pharmacology, Ganglia, Spinal metabolism, Spinal Cord Injuries pathology, TRPM Cation Channels metabolism
- Abstract
Introduction: We sought to determine the contribution of oxidative stress-dependent activation of TRPM2 and L-type voltage-gated Ca(2+) channels (VGCC) in dorsal root ganglion (DRG) neurons of rats after spinal cord injury (SCI)., Methods: The rats were divided into 4 groups: control; sham control; SCI; and SCI+nimodipine groups. The neurons of the SCI groups were also incubated with non-specific TRPM2 channel blockers, 2-aminoethoxydiphenylborate (2-APB) and N-(p-amylcinnamoyl)anthranilic acid (ACA), before H2 O2 stimulation., Results: The [Ca(2+) ]i concentrations were higher in the SCI group than in the control groups, although their concentrations were decreased by nimodipine and 2-APB. The H2 O2 -induced TRPM2 current densities in patch-clamp experiments were decreased by ACA and 2-APB incubation. In the nimodipine group, the TRPM2 channels of neurons were not activated by H2 O2 or cumene hydroperoxide., Conclusions: Increased Ca(2+) influx and currents in DRG neurons after spinal injury indicated TRPM2 and voltage-gated Ca(2+) channel activation., (Copyright © 2013 Wiley Periodicals, Inc.)
- Published
- 2013
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