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Effects of Carbamazepine and Amitriptyline on Tetrodotoxin-resistant $Na^+$ Channels in Immature Rat Trigeminal Ganglion Neurons
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  • Effects of Carbamazepine and Amitriptyline on Tetrodotoxin-resistant $Na^+$ Channels in Immature Rat Trigeminal Ganglion Neurons
  • Effects of Carbamazepine and Amitriptyline on Tetrodotoxin-resistant $Na^+$ Channels in Immature Rat Trigeminal Ganglion Neurons
저자명
Hur. Yun-Kyung,Choi. In-Sun,Cho. Jin-Hwa,Park. Eun-Joo,Choi. Jae-Kap,Choi. Byung-Ju,Jang. Il-Sung
간행물명
Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea
권/호정보
2008년|31권 2호|pp.178-182 (5 pages)
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대한약학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
서지반출

기타언어초록

Although anticonvulsant drugs that block voltage-dependent $Na^+$ channels have been widely used for neuropathic pain, including peripheral nerve injury-induced pain, much less is known about the actions of these drugs on immature trigeminal ganglion (TG) neurons. Here we report the effects of carbamazepine (CBZ) and amitriptyline (ATL) on tetrodotoxin-resistant (TTX-R) $Na^+$ channels expressed on immature rat TG neurons. TTX-R $Na^+$ currents $(I_{Na})$ were recorded in the presence of 300 nM TTX by use of a conventional whole-cell patch clamp method. Both CBZ and ATL inhibited TTX-R $I_{Na}$ in a concentration-dependent manner, but ATL was more potent. While CBZ and ATL did not affect the overall voltage-activation relationship of TTX-R $Na^+$ channels, both drugs shifted the voltage-activation relationship to the left, indicating that they inhibited TTX-R $Na^+$ channels more efficiently at depolarized membrane potentials. ATL showed a profound use-dependent blockade of TTX-R $I_{Na}$, but CBZ had little effect. The present results suggest that both CBZ and ATL, common drugs used for treating neuropathic pain, efficiently inhibit TTX-R $Na^+$ channels expressed on immature TG neurons, and that these drugs might be useful for the treatment of trigeminal nerve injury-induced neuropathic pain, as well as the inhibition of ongoing central sensitization, even during immature periods.