首页> 美国卫生研究院文献>The Journal of Neuroscience >Modulation of Force during Locomotion: Differential Action of Crustacean Cardioactive Peptide on Power-Stroke and Return- Stroke Motor Neurons
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Modulation of Force during Locomotion: Differential Action of Crustacean Cardioactive Peptide on Power-Stroke and Return- Stroke Motor Neurons

机译:运动过程中的力调节:甲壳类强心肽对中风和中风运动神经元的差异作用。

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摘要

Crustacean cardioactive peptide (CCAP) elicited expression of the motor pattern that drives coordinated swimmeret beating in crayfish and modulated this pattern in a dose-dependent manner. In each ganglion that innervates swimmerets, neurons with CCAP-like immunoreactivity sent processes to the lateral neuropils, which contain branches of swimmeret motor neurons and the local pattern-generating circuits.CCAP affected each of the four functional groups of motor neurons, power-stroke excitors (PSE), return-stroke excitors (RSE), power-stroke inhibitors (PSI), and return-stroke inhibitors (RSI), that innervate each swimmeret. When CCAP was superfused, the membrane potentials of these neurons began to oscillate periodically about their mean potentials. The mean potentials of PSE and RSI neurons depolarized, and some of these neurons began to fire during each depolarization. Both intensity and durations of PSE bursts increased significantly. The mean potentials of RSE and PSI neurons hyperpolarized, and these neurons were less likely to fire during each depolarization. When CCAP was superfused in a low Ca2+ saline that blocked chemical transmission, these changes in mean potential persisted, but the periodic oscillations disappeared.These results are evidence that CCAP acts at two levels: activation of local premotor circuits and direct modulation of swimmeret motor neurons. The action on motor neurons is differential; PSEs and RSIs are excited, but RSEs and PSIs are inhibited. The consequences of this selectivity are to increase intensity of bursts of impulses that excite power-stroke muscles.
机译:甲壳类的心脏活性肽(CCAP)引起运动模式的表达,该运动模式驱动小龙虾中的协同游动的跳动并以剂量依赖性方式调节这种模式。在每个支配游泳者的神经节中,具有CCAP样免疫反应性的神经元将过程发送至外侧神经枕,其中包含游泳者运动神经元的分支和局部模式产生电路.CCAP影响运动神经元的四个功能组中的每一个刺激(PSE),回泳兴奋剂(RSE),中风抑制器(PSI)和回程抑制器(RSI),它们可支配每个游泳者。当CCAP被融合时,这些神经元的膜电位开始围绕其平均电位周期性地振荡。 PSE和RSI神经元的平均电位已去极化,并且在每次去极化过程中,其中一些神经元开始激发。 PSE爆发的强度和持续时间均显着增加。 RSE和PSI神经元的平均电位超极化,并且在每次去极化过程中这些神经元发射的可能性较小。当CCAP在低Ca 2 + 盐水中进行融合以阻止化学物质传播时,这些平均电势的变化持续存在,但周期性振荡消失了。这些结果证明CCAP在两个水平上起作用:运动前回路和游泳运动神经元的直接调节。对运动神经元的作用是不同的。 PSE和RSI被激发,但是RSE和PSI被抑制。这种选择性的结果是增加了激发中风肌肉的脉冲爆发的强度。

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