| dc.creator |
UGUZ, Abdulhadi Cihangir |
|
| dc.creator |
BORCAK, Muhammed |
|
| dc.creator |
Cig, Bilal |
|
| dc.creator |
ÖZGÜL, Cemil |
|
| dc.creator |
İSMAİLOĞLU, Özgür |
|
| dc.creator |
NAZIROĞLU, Mustafa |
|
| dc.date |
2013-11-30T22:00:00Z |
|
| dc.date.accessioned |
2020-10-06T12:03:28Z |
|
| dc.date.available |
2020-10-06T12:03:28Z |
|
| dc.identifier |
fcf48fd2-0f8c-4de1-8707-95556c4445f8 |
|
| dc.identifier |
10.1002/mus.23844 |
|
| dc.identifier |
https://avesis.sdu.edu.tr/publication/details/fcf48fd2-0f8c-4de1-8707-95556c4445f8/oai |
|
| dc.identifier.uri |
http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/77039 |
|
| dc.description |
Introduction: We sought to determine the contribution of oxidative stress-dependent activation of TRPM2 and L-type voltage-gated Ca2+ 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 H2O2 stimulation. Results:The [Ca2+](i) concentrations were higher in the SCI group than in the control groups, although their concentrations were decreased by nimodipine and 2-APB. The H2O2-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 H2O2 or cumene hydroperoxide. Conclusions: Increased Ca2+ influx and currents in DRG neurons after spinal injury indicated TRPM2 and voltage-gated Ca2+ channel activation. Muscle Nerve48: 945-950, 2013 |
|
| dc.language |
eng |
|
| dc.rights |
info:eu-repo/semantics/closedAccess |
|
| dc.title |
ROLE OF TRPM2 CATION CHANNELS IN DORSAL ROOT GANGLION OF RATS AFTER EXPERIMENTAL SPINAL CORD INJURY |
|
| dc.type |
info:eu-repo/semantics/article |
|