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首页> 外文期刊>Journal of receptor and signal transduction research >Modulation of action potential and calcium signaling by levetiracetam in rat sensory neurons
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Modulation of action potential and calcium signaling by levetiracetam in rat sensory neurons

机译：左乙拉西坦在大鼠感觉神经元中对动作电位和钙信号的调节

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Levetiracetam (LEV), a new anticonvulsant agent primarily used to treat epilepsy, has been used in pain treatment but the cellular mechanism of this action remains unclear. This study aimed to investigate effects of LEV on the excitability and membrane depolarization-induced calcium signaling in isolated rat sensory neurons using the whole-cell patch clamp and fura 2based ratiometric Ca ~(2+)-imaging techniques. Dorsal root ganglia (DRG) were excised from neonatal rats, and cultured following enzymatic and mechanical dissociation. Under current clamp conditions, acute application of LEV (30 M, 100 M and 300 M) significantly increased input resistance and caused the membrane to hyperpolarize from resting membrane potential in a dose-dependent manner. Reversal potentials of action potential (AP) after hyperpolarising amplitudes were shifted to more negative, toward to potassium equilibrium potentials, after application of LEV. It also caused a decrease in number of APs in neurons fired multiple APs in response to prolonged depolarization. Fura-2 fluorescence Ca ~(2+) imaging protocols revealed that HiK + (30 mM)-induced intracellular free Ca ~(2+) ([Ca ~(2+)]i) was inhibited to 97.8 ± 4.6% (n = 17), 92.6 ± 4.8% (n = 17, p < 0.01) and 89.1 ± 5.1% (n = 18, p < 0.01) after application of 30 M, 100 M and 300 M LEV (respectively), without any significant effect on basal levels of [Ca ~(2+)]i. This is the first evidence for the effect of LEV on the excitability of rat sensory neurons through an effect which might involve activation of potassium channels and inhibition of entry of Ca 2+, providing new insights for cellular mechanism(s) of LEV in pain treatment modalities.
机译：左乙拉西坦（LEV）是一种主要用于治疗癫痫的新型抗惊厥药，已用于疼痛治疗，但该作用的细胞机制尚不清楚。本研究旨在研究LEV对全细胞膜片钳和基于Fura 2的比例Ca〜（2+）成像技术对离体大鼠感觉神经元的兴奋性和膜去极化诱导的钙信号的影响。从新生大鼠中切除背根神经节（DRG），并在酶和机械解离后进行培养。在当前钳位条件下，急性应用LEV（30 M，100 M和300 M）会显着增加输入电阻，并导致膜从静息膜电位以剂量依赖方式超极化。施加LEV后，超极化幅度后动作电位（AP）的逆转电位向负值转移，移向钾平衡电位。这也导致响应长时间去极化而发射多个AP的神经元中AP的数量减少。 Fura-2荧光Ca〜（2+）成像方案显示，HiK +（30 mM）诱导的细胞内游离Ca〜（2+）（[Ca〜（2 +）] i）被抑制至97.8±4.6％（n分别施加30 M，100 M和300 M LEV后= 92.6±4.8％（n = 17，p <0.01）和89.1±5.1％（n = 18，p <0.01），无显着性对[Ca〜（2 +）] i基础水平的影响。这是LEV对大鼠感觉神经元兴奋性影响的第一个证据，其作用可能涉及激活钾离子通道和抑制Ca 2+的进入，为LEV在疼痛治疗中的细胞机制提供了新见解。方式。

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