NEUROBIOLOGIC STUDIES OF NEURONS AND GLIA IN CELL CULTURE

隔室组织培养系统已被用于控制神经元 活动，以测量定义之间的突触连接的强度 神经元群体和测试假设，涉及的机制， 活动依赖性突触可塑性。突触后电活动， NMDA受体激活和细胞内钙水平在细胞内钙离子浓度变化中相互作用 确定慢性神经毒性引起的突触功效的长期变化， 刺激突触输入。 DRG神经元的轴突生长（生长锥活动）迅速受阻 通过电激活（相位刺激比强直刺激更有效）。 随着长时间的刺激（小时），生长锥可以变得适应 然后继续生长电刺激增加细胞内 生长轴突和生长锥中的钙。这种增长是短暂的 轴突的钙缓冲能力似乎受到调节， 一部分，通过电活动。 BayK 8644可靠地增强高压激活（HVA）钙电流 虽然ω-芋螺毒素在这些电流中产生适度的降低， 培养的小鼠脊髓（SC）和DRG神经元。BayK 8644增强垫块 在少数情况下，这些细胞类型之间的突触相互作用（没有 大多数变化），而ω-芋螺毒素没有可检测到的影响 （ω-芋螺毒素消除了青蛙神经肌肉的突触传递， junction）。我们的研究结果表明，在以下方面存在高度异质性： 负责释放神经递质的钙通道

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.