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Aminoethoxydiphenyl borate and flufenamic acid inhibit Ca2+ influx through TRPM2 channels in rat dorsal root ganglion neurons activated by ADP-ribose and rotenone.
J Membr Biol. 2011 May; 241(2):69-75.JM

Abstract

Exposure to oxidative stress causes health problems, including sensory neuron neuropathy and pain. Rotenone is a toxin used to generate intracellular oxidative stress in neurons. However, the mechanism of toxicity in dorsal root ganglion (DRG) neurons has not been characterized. Melastatin-like transient receptor potential 2 (TRPM2) channel activation and inhibition in response to oxidative stress, ADP-ribose (ADPR), flufenamic acid (FFA) and 2-aminoethoxydiphenyl borate (2-APB) in DRG neurons are also not clear. We tested the effects of FFA and 2-APB on ADPR and rotenone-induced TRPM2 cation channel activation in DRG neurons of rats. DRG neurons were freshly isolated from rats and studied with the conventional whole-cell patch-clamp technique. Rotenone, FFA and 2-APB were extracellularly added through the patch chamber, and ADPR was applied intracellularly through the patch pipette. TRPM2 cation currents were consistently induced by ADPR and rotenone. Current densities of the neurons were higher in the ADPR and rotenone groups than in control. The time courses (gating times) in the neurons were longer in the rotenone than in the ADPR group. ADPR and rotenone-induced TRPM2 currents were totally blocked by 2-APB and partially blocked by FFA. In conclusion, TRPM2 channels were constitutively activated by ADPR and rotenone, and 2-APB and FFA induced an inhibitory effect on TRPM2 cation channel currents in rat DRG neurons. Since oxidative stress is a common feature of neuropathic pain and diseases of sensory neurons, the present findings have broad application to the etiology of neuropathic pain and diseases of DRG neurons.

Authors+Show Affiliations

Department of Biophysics, Faculty of Medicine, University of Suleyman Demirel, 32260, Isparta, Turkey. mnaziroglu@med.sdu.edu.trNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

21509529

Citation

Nazıroğlu, Mustafa, et al. "Aminoethoxydiphenyl Borate and Flufenamic Acid Inhibit Ca2+ Influx Through TRPM2 Channels in Rat Dorsal Root Ganglion Neurons Activated By ADP-ribose and Rotenone." The Journal of Membrane Biology, vol. 241, no. 2, 2011, pp. 69-75.
Nazıroğlu M, Özgül C, Çelik Ö, et al. Aminoethoxydiphenyl borate and flufenamic acid inhibit Ca2+ influx through TRPM2 channels in rat dorsal root ganglion neurons activated by ADP-ribose and rotenone. J Membr Biol. 2011;241(2):69-75.
Nazıroğlu, M., Özgül, C., Çelik, Ö., Çiğ, B., & Sözbir, E. (2011). Aminoethoxydiphenyl borate and flufenamic acid inhibit Ca2+ influx through TRPM2 channels in rat dorsal root ganglion neurons activated by ADP-ribose and rotenone. The Journal of Membrane Biology, 241(2), 69-75. https://doi.org/10.1007/s00232-011-9363-9
Nazıroğlu M, et al. Aminoethoxydiphenyl Borate and Flufenamic Acid Inhibit Ca2+ Influx Through TRPM2 Channels in Rat Dorsal Root Ganglion Neurons Activated By ADP-ribose and Rotenone. J Membr Biol. 2011;241(2):69-75. PubMed PMID: 21509529.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aminoethoxydiphenyl borate and flufenamic acid inhibit Ca2+ influx through TRPM2 channels in rat dorsal root ganglion neurons activated by ADP-ribose and rotenone. AU - Nazıroğlu,Mustafa, AU - Özgül,Cemil, AU - Çelik,Ömer, AU - Çiğ,Bilal, AU - Sözbir,Ercan, Y1 - 2011/04/21/ PY - 2011/03/13/received PY - 2011/03/21/accepted PY - 2011/4/22/entrez PY - 2011/4/22/pubmed PY - 2011/9/13/medline SP - 69 EP - 75 JF - The Journal of membrane biology JO - J Membr Biol VL - 241 IS - 2 N2 - Exposure to oxidative stress causes health problems, including sensory neuron neuropathy and pain. Rotenone is a toxin used to generate intracellular oxidative stress in neurons. However, the mechanism of toxicity in dorsal root ganglion (DRG) neurons has not been characterized. Melastatin-like transient receptor potential 2 (TRPM2) channel activation and inhibition in response to oxidative stress, ADP-ribose (ADPR), flufenamic acid (FFA) and 2-aminoethoxydiphenyl borate (2-APB) in DRG neurons are also not clear. We tested the effects of FFA and 2-APB on ADPR and rotenone-induced TRPM2 cation channel activation in DRG neurons of rats. DRG neurons were freshly isolated from rats and studied with the conventional whole-cell patch-clamp technique. Rotenone, FFA and 2-APB were extracellularly added through the patch chamber, and ADPR was applied intracellularly through the patch pipette. TRPM2 cation currents were consistently induced by ADPR and rotenone. Current densities of the neurons were higher in the ADPR and rotenone groups than in control. The time courses (gating times) in the neurons were longer in the rotenone than in the ADPR group. ADPR and rotenone-induced TRPM2 currents were totally blocked by 2-APB and partially blocked by FFA. In conclusion, TRPM2 channels were constitutively activated by ADPR and rotenone, and 2-APB and FFA induced an inhibitory effect on TRPM2 cation channel currents in rat DRG neurons. Since oxidative stress is a common feature of neuropathic pain and diseases of sensory neurons, the present findings have broad application to the etiology of neuropathic pain and diseases of DRG neurons. SN - 1432-1424 UR - https://www.unboundmedicine.com/medline/citation/21509529/Aminoethoxydiphenyl_borate_and_flufenamic_acid_inhibit_Ca2+_influx_through_TRPM2_channels_in_rat_dorsal_root_ganglion_neurons_activated_by_ADP_ribose_and_rotenone_ L2 - https://dx.doi.org/10.1007/s00232-011-9363-9 DB - PRIME DP - Unbound Medicine ER -