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Clione limacina 翼足类软体动物游泳加速的细胞机制。

Cellular Mechanisms Underlying Swim Acceleration in the Pteropod Mollusk Clione limacina.

机构信息

Abilene Christian University, Biology Department, Abilene, Texas 79699-7868.

出版信息

Integr Comp Biol. 2004 Feb;44(1):37-46. doi: 10.1093/icb/44.1.37.

Abstract

The pteropod mollusk Clione limacina swims by dorsal-ventral flapping movements of its wing-like parapodia. Two basic swim speeds are observed-slow and fast. Serotonin enhances swimming speed by increasing the frequency of wing movements. It does this by modulating intrinsic properties of swim interneurons comprising the swim central pattern generator (CPG). Here we examine some of the ionic currents that mediate changes in the intrinsic properties of swim interneurons to increase swimming speed in Clione. Serotonin influences three intrinsic properties of swim interneurons during the transition from slow to fast swimming: baseline depolarization, postinhibitory rebound (PIR), and spike narrowing. Current clamp experiments suggest that neither I(h) nor I(A) exclusively accounts for the serotonin-induced baseline depolarization. However, I(h) and I(A) both have a strong influence on the timing of PIR-blocking I(h) increases the latency to PIR while blocking I(A) decreases the latency to PIR. Finally, apamin a blocker of I(K(Ca)) reverses serotonin-induced spike narrowing. These results suggest that serotonin may simultaneously enhance I(h) and I(K(Ca)) and suppress I(A) to contribute to increases in locomotor speed.

摘要

翼足目软体动物 Clione limacina 通过其翼状副肢的背-腹拍打运动来游泳。观察到两种基本的游泳速度-慢和快。血清素通过增加翅膀运动的频率来提高游泳速度。它通过调节构成游泳中枢模式发生器(CPG)的游泳中间神经元的固有特性来实现这一点。在这里,我们研究了一些介导游泳中间神经元固有特性变化以增加 Clione 游泳速度的离子电流。血清素在从慢泳到快泳的转变过程中影响游泳中间神经元的三个固有特性:基线去极化、后抑制反弹(PIR)和尖峰变窄。电流钳实验表明,I(h)和 I(A)都不能单独解释血清素诱导的基线去极化。然而,I(h)和 I(A)都对 PIR 的时间有很大的影响-阻断 I(h)增加了 PIR 的潜伏期,而阻断 I(A)则降低了 PIR 的潜伏期。最后,apamin 是 I(K(Ca))的阻断剂,可逆转血清素诱导的尖峰变窄。这些结果表明,血清素可能同时增强 I(h)和 I(K(Ca))并抑制 I(A),以促进运动速度的提高。

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