How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.
How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.
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DOI：
10.3389/fncel.2014.00040
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发表时间：
2014
影响因子：
5.3
通讯作者：
Frank CA
中科院分区：
文献类型：
--
作者：
Frank CA
在整个生命过程中，动物面临着各种各样的挑战，如发育发育、毒素的存在或温度的变化。神经元回路和突触通过执行一系列神经可塑性范例来应对挑战。一些范式允许神经元上调或下调活动输出，而与之相反的范式则确保输出保持在适当的生理范围内。越来越多的证据表明，稳态突触可塑性(HSP)在后一种情况下是至关重要的。电压门控钙通道门控形式的HSP。在突触前，综合数据显示，当突触活性减弱时，稳态信号系统可以通过增加突触前CaV2类通道的钙内流来纠正损伤。钙离子内流的增加通常伴随着活动区的大小和突触前小泡池的大小平行增加。这些变化与神经递质释放的动态平衡增强相吻合。在突触后，有大量证据表明，通过CaV1-型钙通道减少网络活动和钙内流的损失也会导致适应性内稳信号。一些适应性通过逆行信号和突触后神经递质受体的从头插入来驱动突触前囊泡池大小和周转率的增强。在网络激活或单细胞刺激后，通过CaV1增加钙内流可以引起相反的反应-通过移除兴奋性受体来抑制动态平衡。在热休克蛋白和钙离子通道病之间存在有趣的联系--例如癫痫、偏头痛、共济失调和肌无力。其中一些疾病的间歇性特征表明功能稳定和不稳定的交替周期。揭示有关钙通道是如何在HSP的背景下调节的信息，可能与理解这些和其他疾病有关。
Throughout life, animals face a variety of challenges such as developmental growth, the presence of toxins, or changes in temperature. Neuronal circuits and synapses respond to challenges by executing an array of neuroplasticity paradigms. Some paradigms allow neurons to up- or downregulate activity outputs, while countervailing ones ensure that outputs remain within appropriate physiological ranges. A growing body of evidence suggests that homeostatic synaptic plasticity (HSP) is critical in the latter case. Voltage-gated calcium channels gate forms of HSP. Presynaptically, the aggregate data show that when synapse activity is weakened, homeostatic signaling systems can act to correct impairments, in part by increasing calcium influx through presynaptic CaV2-type channels. Increased calcium influx is often accompanied by parallel increases in the size of active zones and the size of the readily releasable pool of presynaptic vesicles. These changes coincide with homeostatic enhancements of neurotransmitter release. Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling. Some adaptations drive presynaptic enhancements of vesicle pool size and turnover rate via retrograde signaling, as well as de novo insertion of postsynaptic neurotransmitter receptors. Enhanced calcium influx through CaV1 after network activation or single cell stimulation can elicit the opposite response—homeostatic depression via removal of excitatory receptors. There exist intriguing links between HSP and calcium channelopathies—such as forms of epilepsy, migraine, ataxia, and myasthenia. The episodic nature of some of these disorders suggests alternating periods of stable and unstable function. Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.
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