Yazarlar |
Mustafa Nazıroğlu
Süleyman Demirel Üniversitesi, Türkiye |
Abdülhadi Cihangir Uğuz
Süleyman Demirel Üniversitesi, Türkiye |
Özgür İsmailoğlu
|
Doç. Dr. Bilal ÇİĞ
Süleyman Demirel Üniversitesi, Türkiye |
Cemil Özgül
|
Muhammed Borcak
|
Özet |
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 |
Anahtar Kelimeler |
Ca2+ signaling | nimodipine | oxidative stress | peripheral pain | spinal injury | TRPM2 cation channels |
Makale Türü | Özgün Makale |
Makale Alt Türü | SSCI, AHCI, SCI, SCI-Exp dergilerinde yayımlanan tam makale |
Dergi Adı | MUSCLE & NERVE |
Dergi ISSN | 0148-639X |
Dergi Tarandığı Indeksler | SCI-Expanded |
Makale Dili | İngilizce |
Basım Tarihi | 12-2013 |
Cilt No | 48 |
Sayı | 6 |
Sayfalar | 945 / 950 |
Doi Numarası | 10.1002/mus.23844 |
Makale Linki | http://doi.wiley.com/10.1002/mus.23844 |