Role of TRPM2 cation channels in dorsal root ganglion of rats after experimental spinal cord injury
    
Yazarlar (6)
Mustafa Nazıroğlu Süleyman Demirel Üniversitesi, Türkiye
Abdülhadi Cihangir Uğuz Suleyman Demirel University, Türkiye
Özgür İsmailoğlu Suleyman Demirel University, Türkiye
Doç. Dr. Bilal ÇİĞ Suleyman Demirel University, Türkiye
Cemil Özgül Suleyman Demirel University, Türkiye
Muhammed Borcak Suleyman Demirel University, Türkiye
Makale Türü Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale)
Dergi Adı Muscle Nerve
Dergi ISSN 1097-4598 Wos Dergi Scopus Dergi
Dergi Tarandığı Indeksler SCI-Expanded
Makale Dili İngilizce Basım Tarihi 12-2013
Cilt / Sayı / Sayfa 48 / 6 / 945–950 DOI 10.1002/mus.23844
Makale Linki https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/mus.23844
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