通过改变突触前钙离子内流实现的平衡型突触可塑性。
Homeostatic synaptic plasticity through changes in presynaptic calcium influx.
机构信息
Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 0QH, United Kingdom.
出版信息
J Neurosci. 2011 May 18;31(20):7492-6. doi: 10.1523/JNEUROSCI.6636-10.2011.
Abstract
Chronic perturbations of electrical activity within neural circuits lead to compensatory changes in synaptic strength collectively termed homeostatic synaptic plasticity. The postsynaptic mechanisms underlying these modifications have been characterized in some detail, but the presynaptic mechanisms that alter the efficiency of evoked neurotransmitter release are less clear. To investigate the role of presynaptic calcium influx, we have combined the use of two fluorescent proteins in cultured hippocampal neurons: a calcium reporter localized to synaptic vesicles, SyGCaMP2, and a reporter of vesicle fusion, SypHy. We find that a decrease in the activity of the network causes an increase in the amount of calcium entering the synaptic bouton in response to an action potential and an increase in the probability of vesicle fusion. Homeostatic changes in release probability varied as the third power of calcium influx. These results indicate that changes in the number and/or function of presynaptic calcium channels are major determinants of homeostatic changes in synaptic strength.
摘要
神经回路中电活动的慢性干扰会导致突触强度的代偿性变化，通常被称为同型突触可塑性。这些修饰的突触后机制已经被详细描述，但改变诱发神经递质释放效率的突触前机制还不太清楚。为了研究突触前钙内流的作用，我们在培养的海马神经元中结合使用了两种荧光蛋白：一种定位于突触囊泡的钙报告蛋白 SyGCaMP2 和囊泡融合的报告蛋白 SypHy。我们发现，网络活动的减少会导致动作电位引起的突触末梢进入的钙量增加，并增加囊泡融合的概率。释放概率的同型变化与钙内流的立方成正比。这些结果表明，突触前钙通道数量和/或功能的变化是突触强度同型变化的主要决定因素。
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