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The slow sodium influx educed by veratridine and the calcium-dependent potassium outflux are regarded as the two slow variables, which are responsible for the parabolic bursting.

结合实验模型，从离子通道活动的角度揭示了抛物线簇放电发生的生物物理机制。由藜芦碱诱发的慢变钠内流和钙依赖钾外流被认为是引发实验所观察到的抛物线簇放电的两个慢变量。

The effects of phenytoin (2.5, 5, 10 and l5 μmol/L) and gabapentin (2.5, 5 and l0μ mol/L) on the epileptiform activity were observed under the volt age- clamp configuration. and the current changes for 1 hour in CA I neurons was also observed. Results Nine-sixteen minutes after veratridine perfusion, the huge.

分别在电压钳模式下观察2.5、5、10、15μmol/L苯妥英和2.5、5、10μmol/L加巴喷丁对这种癫痫活动的影响；测定藜芦碱灌流后CA1锥体神经元Ih电流的变化规律。

However, the role of inactivation gate of sodium channel is not clear. In present study, single fibre recording in vivo from dorsal root on chronically compressed DRG model was used. We analyzed the characters of ISI series of oscillation firing of type A neurons induced by veratridine, an inhibitor of inactivation gate of sodium channel.

本研究在大鼠背根节慢性压迫模型上，利用在体单纤维记录方法，观察与分析Na通道失活门抑制剂藜芦碱引起受损背根节A类神经元放电ISI序列发生的变化特征，为了解Na通道失活门与放电型式的关系以及进一步探索放电时间型式与疼痛的关系奠定基础。

Low-dosage veratridine may induce runs of PDS like epileptiform activities on rat CA1 pyramidal neurons.

小剂量藜芦碱可在大鼠脑海马CA1区锥体神经元上诱发出阵发性去极化漂移样癫痫活动。

Recertly, the intrinsic nature of PDS has received more attention.OBJECTIVE: To observe the characteristics of epileptiform activities of rat hippocampal CA1 pyramidal neurons induced by low-dosage veratridine and investigate its possible ion mechanism.

近年来，阵发性去极化漂移的内因机制得到进一步关注和重视。；目的：观察小剂量藜芦碱诱发大鼠脑海马CA1区锥体神经元产生癫痫样活动的特征，探讨其可能的离子机制。

Furthermore, the roles that veratridine plays in the emergence of the parabolic bursting, namely inhibiting the inactivation of sodium channels and eliciting the slow sodium influx, are clarified.

进而阐明了藜芦碱引起这一放电形式所起的作用，即抑制钠通道失活引发慢变钠内流。这种利用非线性动力学理论的分析方法可能会为分析药物的药物动力学提供一种新的途径。

RESULTS: After perfusion of 0.5 μmol/L veratridine, the rat pyramidal neurons in CA1 area displayed relatively fixed-mode of runs of PDS bursting, followed by the hyperpolarization of cell membrane.

小剂量藜芦碱可在大鼠脑海马CA1区锥体神经元上诱发出阵发性去极化漂移样癫痫活动。

BmK IT2 associateed with and dissociated from its binding sites on insect synaptosomes quickly in two phase kinetic manner, and its specific binding was independence of membrane potential, but could be significantly inhibited by native BmK IT2, BmK AS and BmK AS-1 in a dose-dependent manner, and only partially by BmK Ⅰ or veratridine at high concentration.

BmK IT2能以两相动力学方式快速与昆虫突触体结合和解离，且其结合不依赖于膜电位，可分别被天然毒素BmK IT2，BmK AS和BmK AS-1剂量依赖地抑制，另也可被高浓度BmK Ⅰ和藜芦碱部分抑制。

In the same neuron, veratridine (1.5～5.0 μmol/L) caused slow wave oscillations of interspike intervals, while aconitine (10～200 μmol/L) caused tonic firing.

结果发现，在同一神经元，藜芦碱(1.5～5.0 μmol/L)可以引起放电峰峰间期的慢波振荡，即峰峰间期由大逐渐减小，然后又逐渐增大，形成重复的振荡波形，每个振荡持续约数十秒至数分钟；而乌头碱(10～200 μmol/L)则引起强直性放电，即峰峰间期逐渐减小，然后维持在一个稳定的水平。

Methods By means of whole-cell patch clamp technique, the epileptiform discharge model of rats hippocampal CA1 neurons was constructed with extracellular perfusion of 0.5 μmol/L veratridine, and the model should be regarded as successfully estabilshed if bursting discharge emerged within 30 min perfusion.

通过膜片钳全细胞记录技术，胞外灌流0.5μmol/L藜芦碱，制作大鼠海马CA1锥体神经元癫痫样放电模型，如果在灌流30min内出现振荡样放电，即认为造模成功。

With Death guitarist Schuldiner adopting vocal duties, the band made a major impact on the scene.

随着死亡的吉他手Schuldiner接受主唱的职务，乐队在现实中树立了重要的影响。

But he could still end up breakfasting on Swiss-government issue muesli because all six are accused of nicking around 45 million pounds they should have paid to FIFA.

不过他最后仍有可能沦为瑞士政府&议事餐桌&上的一道早餐，因为这所有六个人都被指控把本应支付给国际足联的大约4500万英镑骗了个精光。