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veratridine相关的网络例句

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与 veratridine 相关的网络例句 [注:此内容来源于网络,仅供参考]

The firing patterns induced by veratridine and aconitine, inhibitors of inactivation gate of sodium channel operating on different binding sites, were compared.

藜芦碱和乌头碱是钠通道失活门的抑制剂,但二者作用于不同的位点,前者结合于D2-S6,后者结合于D3-S6。我们比较了这两种试剂引发的放电模式。

In addition, the binding of BmK abT to Heliothis nerve cord synaptosomes was significantly enhanced by increasing the membrane potential and veratridine concentration and was inhibited by BmK IT2, but not by BmK AS or BmK I.

研究结果提示BmK abT 可以作为一个独特的新型钠通道调制剂探针用于深入研究电压门控钠通道的亚型、结构特征和功能特性。

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。

The binding of BmK abT to rat brain synaptosomes could be partially inhibited by increasing the membrane potential, but not by BmK AS, BmK IT2 and BmK I. Binding was not modulated by veratridine.

对于哺乳动物脑型钠通道,BmK abT 的结合位点可能不同于BmK AS、BmK IT2 和BmK I 的结合位点,但与经典的α-型毒素结合位点较为接近;对于昆虫钠通道,BmK abT 的结合位点至少部分与抑制型抗昆虫毒素BmK IT2 的结合位点相互重叠。

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。

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