N-Ethylmaleimide modulation of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels in rat dorsal root ganglion neurons
- Authors
- Song, Jin-Ho; Jang, Yoon Young; Shin, Yong Kyoo; Lee, Chung-Soo; Chung, Sungkwon
- Issue Date
- Feb-2000
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- N-ethylmaleimide; sulfhydryl; alkylation; tetrodotoxin-sensitive; tetrodotoxin-resistant; sodium channel; dorsal root ganglion
- Citation
- BRAIN RESEARCH, v.855, no.2, pp 267 - 273
- Pages
- 7
- Journal Title
- BRAIN RESEARCH
- Volume
- 855
- Number
- 2
- Start Page
- 267
- End Page
- 273
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/47384
- DOI
- 10.1016/S0006-8993(99)02405-1
- ISSN
- 0006-8993
1872-6240
- Abstract
- The effects of N-ethylmaleimide (NEM), an alkylating reagent to protein sulfhydryl groups, on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in rat, dorsal root ganglion (DRG) neurons were studied using the whole cell configuration of patch-clamp technique. When currents were evoked by step depolarizations to 0 mV from a holding potential of -80 mV NEM decreased the amplitude of TTX-S sodium current, but exerted little or no effect on that of TTX-R sodium current. The inhibitory effect of NEM on TTX-S sodium channel was mainly due to the shift of the steady-stare inactivation curve in the hyperpolarizing direction. NEM did not affect the voltage-dependence of the activation of TTX-S sodium channel. The steady-state inactivation curve for TTX-R sodium channel was shifted by NEM in the hyperpolarizing direction as that for TTX-S sodium channel. NEM caused a change in the voltage-dependence of the activation of TTX-R sodium channel unlike TTX-S sodium channel. After NEM treatment, the amplitudes of TTX-R sodium currents at test voltages below -10 mV were increased, but those at more positive voltages were not affected, This was explained by the shift in the conductance-voltage curve for TTX-R sodium channels in the hyperpolarizing direction after NEM treatment. (C) 2000 Elsevier Science B.V. All rights reserved.
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