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Role of TRPM2 cation channels in dorsal root ganglion of rats after experimental spinal cord injury
Author(s) -
Naziroğlu Mustafa,
Uğuz Abdülhadi Cihangir,
Ismailoğlu Özgür,
Çiğ Bilal,
Özgül Cemil,
Borcak Muhammed
Publication year - 2013
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.23844
Subject(s) - dorsal root ganglion , trpm2 , nimodipine , spinal cord , chemistry , spinal cord injury , transient receptor potential channel , endocrinology , anesthesia , medicine , neuroscience , pharmacology , calcium , biochemistry , biology , receptor
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 H 2 O 2 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 H 2 O 2 ‐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 H 2 O 2 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. Muscle Nerve 48 : 945–950, 2013