Carlin K P, Jones K E, Jiang Z, Jordan L M, Brownstone R M
Departments of Surgery and Physiology, University of Manitoba, 730 William Avenue, Winnipeg, MB, Canada R3E 3J7.
Eur J Neurosci. 2000 May;12(5):1635-46. doi: 10.1046/j.1460-9568.2000.00055.x.
The intrinsic properties of mammalian spinal motoneurons provide them with the capability to produce high rates of sustained firing in response to transient inputs (bistability). Even though it has been suggested that a persistent dendritic calcium current is responsible for the depolarizing drive underlying this firing property, such a current has not been demonstrated in these cells. In this study, calcium currents are recorded from functionally mature mouse spinal motoneurons using somatic whole-cell patch-clamp techniques. Under these conditions a component of the current demonstrated kinetics consistent with a current originating at a site spatially segregated from the soma. In response to step commands this component was seen as a late-onset, low amplitude persistent current whilst in response to depolarizing-repolarizing ramp commands a low voltage clockwise current hysteresis was recorded. Simulations using a neuromorphic motoneuron model could reproduce these currents only if a noninactivating calcium conductance was placed in the dendritic compartments. Pharmacological studies demonstrated that both the late-onset and hysteretic currents demonstrated sensitivity to both dihydropyridines and the L-channel activator FPL-64176. Furthermore, the alpha1D subunits of L-type calcium channels were immunohistochemically demonstrated on motoneuronal dendrites. It is concluded that there are dendritically located L-type channels in mammalian motoneurons capable of mediating a persistent depolarizing drive to the soma and which probably mediate the bistable behaviour of these cells.
哺乳动物脊髓运动神经元的内在特性使其能够在受到短暂输入时产生高频率的持续放电(双稳性)。尽管有人提出持续性树突钙电流是这种放电特性背后去极化驱动的原因,但尚未在这些细胞中证实存在这样一种电流。在本研究中,使用体细胞全细胞膜片钳技术从功能成熟的小鼠脊髓运动神经元记录钙电流。在这些条件下,电流的一个成分表现出的动力学与起源于与胞体空间分离部位的电流一致。响应阶跃指令时,该成分表现为迟发、低幅度的持续电流,而响应去极化 - 复极化斜坡指令时,记录到低电压顺时针电流滞后现象。仅当在树突区室中放置非失活钙电导时,使用神经形态运动神经元模型进行的模拟才能重现这些电流。药理学研究表明,迟发电流和滞后电流对二氢吡啶类药物和L型通道激活剂FPL - 64176均敏感。此外,免疫组织化学证明运动神经元树突上存在L型钙通道的α1D亚基。结论是,哺乳动物运动神经元中存在位于树突的L型通道,能够介导对胞体的持续去极化驱动,并且可能介导这些细胞的双稳性行为。