Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity
Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity
复制标题
DOI：
10.1016/j.neuron.2004.11.013
复制
发表时间：
2004-12-02
期刊：
影响因子：
16.2
通讯作者：
Liu, GS
中科院分区：
文献类型：
--
作者：
Slutsky, I;Sadeghpour, S;Liu, GS
神经回路中突触的可塑性受活动的调节，但其潜在的机制仍然难以捉摸。使用染料FM 1 -43直接成像突触前功能，我们发现，大量的突触前末梢在海马培养物中具有较低的释放概率。虽然这些终端是不容易修改的，一个短暂的，但不是永久的长期减少网络活动或Ca 2+内流可以增加其modifiability。这种调制的可塑性介导的Ca 2+流量通过NMDA和电压门控钙通道，并在48小时内丢失。一个更持久的增强突触可塑性实现了通过选择性地减少与不相关的活动通过调整电压依赖性Mg 2+块的NMDAR相关的Ca 2+流量。由该处理诱导的含NR 2B的NMDAR的上调是可塑性增强的重要但不是唯一贡献者。因此，活动的数量和质量对神经元的内在可塑性有不同的影响。
The plasticity of synapses within neural circuits is regulated by activity, but the underlying mechanisms remain elusive. Using the dye FM1-43 to directly image presynaptic function, we found that large numbers of presynaptic terminals in hippocampal cultures have a low release probability. While these terminals were not readily modifiable, a transient but not permanent long-term reduction of network activity or Ca2+ influx could increase their modifiability. This modulation of plasticity was mediated by Ca2+ flux through NMDA and voltage-gated calcium channels and was lost within 48 hr. A more permanent enhancement of synaptic plasticity was achieved by selectively reducing the Ca2+ flux associated with uncorrelated activity via adjustment of the voltage-dependent Mg2+ block of the NMDAR. Upregulation of NR2B-containing NMDARs induced by this treatment is an important but not sole contributor to the enhancement of plasticity. Thus, quantity and quality of activity have differential effects on the intrinsic plasticity of neurons.