NEUROBIOLOGIC STUDIES OF NEURONS AND GLIA IN CELL CULTURE

一种隔室组织培养系统已用于控制神经元 活跃性，以衡量突触连接的强度 神经元群和测试假说，关于参与的机制 依赖活动的突触可塑性。突触后电活动， NMDA受体激活和细胞内钙水平相互作用 慢性脑损伤后突触效能的长期变化 刺激突触输入。 背根神经节神经元的轴突生长(生长锥活动)迅速受阻 通过电刺激(相位性刺激比紧张性刺激更有效)。 随着刺激时间的延长(小时)，生长锥体可以被调节。 并恢复增长。电刺激增加细胞内 生长轴突及其生长锥体中的钙。这一增长是暂时的 轴突的钙缓冲能力似乎受到调节，在 部分，通过电活动。 Bayk 8644可靠地增强高压激活(HVA)钙电流 而omega-conotoxx可使这些电流适度减少。 培养小鼠脊髓(SC)和背根节神经元。Bayk 8644增强版 少数情况下这些细胞类型之间的突触相互作用(无 大多数)，而欧米茄-芋毒素没有检测到的影响 (欧米茄-芋螺毒素消除青蛙神经肌肉的突触传递 交叉点)。我们的结果表明在以下方面存在高度的异质性 与负责神经递质释放的钙通道有关。

A compartmental tissue culture system has been used to control neuronal activity, to measure the strength of synaptic connections between defined neuronal populations and test hypotheses as to the mechanisms involved in activity-dependent synaptic plasticity. Postsynaptic electrical activity, NMDA receptor activation and intracellular calcium levels interact in determining the long term changes in synaptic efficacy produced by chronic stimulation of synaptic inputs. Axonal outgrowth (growth cone activity) from DRG neurons is quickly blocked by electrical activation (phasic stimulation is more effective than tonic). With prolonged stimulation (hours), the growth cone can become accommodated and resume outgrowth. Electrical stimulation increases intracellular calcium in growing axons and their growth cones. The increase is transient and the calcium buffering capacity of axons appears to be regulated, in part, by electrical activity. BayK 8644 reliably augments high-voltage activated (HVA) calcium currents while omega-conotoxin produces a moderate decrease in these currents in cultured mouse spinal cord (SC) and DRG neurons. BayK 8644 augments synaptic interactions between these cell types in a minority of cases (no change in most), while omega-conotoxin is without detectable effect (omega-conotoxin eliminates synaptic transmission at the frog neuromuscular junction). Our results suggest a high degree of heterogeneity with regard to the calcium channels responsible for neurotransmitter release.