氟吡汀(Flupirtine)屬於一種三氨基吡啶 (triaminopyridine) 的藥物，其主要功能被認是為一種中樞性肌肉鬆弛劑和神經保護特性的非阿片類鎮痛劑。此類藥物被用於多種神經興奮性相關疾病，例如癲癇以及神經方面病變所造成的疼痛。先前研究指出氟吡汀可能作為一種NMDA受體的拮抗劑，並且也同時影響GABAA受體的活性。另外亦可透過刺激M型鉀離子通道(M-type K+ channels)，而影響GABAA受體的活性增加。然而，對於氟吡汀以其結構相關的化合物是否可對於類運動神經元細胞上的其他類型的離子通道造成影響，目前仍然有許多疑問。因此，在本篇研究中，我們利用氟吡汀及其他相關化合物來探討對於類運動神經元中上離子通道的作用。細胞膜片箝制技術(patch-clamp technique)用於偵測氟吡汀於類運動神經元細胞(NSC-34 and NG108-15 )中電生理的效用。結果顯示，在NSC-34細胞中氟吡汀使延遲糾正鉀離子電流減少並呈現濃度依賴性，另外也同時提高失活速率。基於公式進一步算出加入氟吡汀後解離常數大約為9.8 μM。然而，加入是NMDA (30 μM)、gabazine (10 μM)亦或是linopirdine (10 μM)並不能回復氟吡汀所造成延遲糾正鉀離子電流的影響。其次，氟吡汀使得不激活曲線向過極化電位平移，然而對其斜率並沒有顯著改變。此外，我們也測量氟吡汀對於M型鉀離子通道是否有效，與先前研究相似，氟吡汀同樣會使M型鉀離子電流增加並且在不影響離子通道進出電荷的情況下，氟吡汀使得激活曲線向左平移。而在另一種類運動神經元細胞NG108-15，結果顯示氟吡汀會使M型鉀離子電流減少並且提高延遲糾正鉀離子電流的不激活速率。總結來說，於本篇研究我們發現氟吡汀會減少延遲糾正鉀離子電流並且同時也會影響M型鉀離子電流，使得M型鉀離子電流增加，在兩者相互之間的作用下最後會使得類運動神經元細胞放電頻率降低。此外，先前研究指出氟吡汀可能會受到GABA或NMDA受體的影響，然而與本篇研究結果顯示氟吡汀造成延遲糾正鉀離子電流的減少並不會受到GABA或NMDA受體的作用。綜合以上結果，氟吡汀的作用可能不單純先前研究指出M型鉀離子通道的影響，另外也會同時受到延遲糾正鉀離子通道的作用。

Flupirtine (Flu) is recognized to be a triaminopyridine that functions as a centrally acting nonopioid analgesic agent with muscle-relaxant and neuroprotective properties. It has been used in multiple actions involving neuronal overexcitability such as epilepsy and neuropathic pain. Previous studies had been reported that Flu might acts as an antagonist of NMDA receptor and show the ability to facilitate the activity of GABAA receptors accompanied by increase stimulation of M-type K+ channels. However, whether Flu and its structurally related compounds can produce any effects on other types of ion current in motor neurons remains largely unclear. In this study, we sought to evaluate possible effects of Flu and other related compounds on ion currents in two types of motor neuron-like cells, the NSC-34 and NG108-15 cells. The patch-clamp technique was applied to investigate the electrophysiological effects in these cells. During cell exposure to Flu, The amplitude of IK(DR) in NSC-34 cells were significantly reduced accompany with the increasing the inactivation rate. Based on minimal binding scheme, the dissociation constant for Flu-mediated increase of IK(DR) inactivation rate was about 9.8 μM. However, neither NMDA (30 μM), gabazine (10 μM), nor linopirdine (10 μM) reversed Flu-induced changes in IK(DR) inactivation. Moreover, the addition of Flu shift the inactivation curve to more hyperpolarized potentials with no change in the slope factor. Consistent with previous observation, the amplitude of M-type K+ current (IK(M)) were increase and produced a leftward shift in the activation curve of IK(M) with no apparent change in the gating charge of this current. In another neuronal cells (NG108-15), addition of Flu would decrease IK(DR) amplitude and enhanced the inactivation rate of IK(DR). Taken together, the results clearly suggest that Flu would produce inhibitory actions on IK(DR) as well as stimulate IK(M), hence decreasing the firing activity on motor neurons if similar results occur in vivo. In addition, Flu-induced block of IK(DR) is not associated with binding to GABA or NMDA receptors and the effects of this compound on K+ channels apparently are not limited to its action on M-type K+ channels.

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