NEUROBIOLOGIC STUDIES OF NEURONS AND GLIA IN CELL CULTURE

电压依赖性钙通道的深度失活 在以下情况下使用电压钳技术演示2赫兹刺激 培养脊髓(SC)Na、K通道受阻的条件 背根神经节(DRG)神经元。这样的失活要多得多 与SC神经元相比，背根神经节中的神经元更为明显。失活依赖于 对稳定的膜电压和进入的钙的量 神经元。因此，DRG似乎不能很好地调节细胞内钙离子 而不是SC神经元对活动相关的钙内流的反应。DRG 与SC相比，神经元维持递质输出的能力也很差 神经元。这种功能缺陷在高外力环境中更加突出。 钙。背根神经节神经元的突触突触相对缺乏 与这种递质输出缺陷相关的线粒体 重复激活。我们提出文中描述的不活跃的对子 早期的报道可能与无效的钙隔离有关。 机械装置。这些机制可能代表着一个长期的来源 突触效能的调节。 二氢吡啶与尼群地平高、低亲和力结合 培养的神经元，但与其对钙通道的阻断作用相反 在肌肉中，尼群地平在微摩尔浓度下几乎没有或 对神经元钙通道无阻断作用。 不同株疱疹病毒对背根神经节神经元的感染不同 对神经元兴奋性机制的高度特异性影响。融合，与 电耦合，可诱导和阻断钠但不能阻断钙 病毒引起的内向而不是外向整改的渠道 感染。防止病毒复制的阿昔洛韦阻止了 病毒对膜特性的影响。 鸡和大鼠的感觉神经元具有电压敏感的钙通道，并且 在这些细胞的一个亚群中，一个大的延长的后尖峰 就会发生去极化。电压钳实验表明，这之后 电位是由于钙敏感的氯化物电导，其 描述了属性。

Profound inactivation of voltage-dependent calcium channels can be demonstrated with 2 Hz stimulation using voltage clamp techniques under conditions where Na and K channels are blocked in cultured spinal cord (SC) and dorsal root ganglion (DRG) neurons. Such inactivation is much more pronounced in DRG as compared to SC neurons. The inactivation is dependent both on steady membrane voltage and on the amount of calcium which enters the neuron. DRG, thus, appears to regulate intracellular calcium less well than SC neurons in response to activity related calcium ingress. DRG neurons also maintain transmitter output very poorly relative to SC neurons. This deficit in function is accentuated in high external calcium. Synaptic boutons of DRG neurons have a relative paucity of mitochondria correlating with this deficit in transmitter output with repetitive activation. We propose that the inactive boutons described in earlier reports may be related to ineffective calcium sequestering mechanisms. These mechanisms may represent one source of long term modulation of synaptic efficacy. Nitrendipine, a dihydropyridine binds with high and low affinity to cultured neurons, but in contrast to its blocking action for Ca++ channels in muscle, nitrendipine, event at micromolar concentrations, has little or no blocking action on neuronal Ca++ channels. Infection of DRG neurons with various strains of herpes virus has different highly specific effects on neuronal excitable mechanisms. Fusion, with electrical coupling, may be induced and blockade of sodium but not calcium channels and of inward but not outward rectification result from viral infection. Acyclovir, which prevents viral replication, blocked the effects of the virus on membrane properties. Chick and rat sensory neurons have voltage-sensitive calcium channels, and in a subpopulation of these cells, a large prolonged post-spike depolarization occurs. Voltage clamp experiments indicate that this after potential is due to a calcium-sensitive chloride conductance whose properties are described.