Assessing the role of calcium-induced calcium release in short-term presynaptic plasticity at excitatory central synapses
Assessing the role of calcium-induced calcium release in short-term presynaptic plasticity at excitatory central synapses
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DOI：
10.1523/jneurosci.22-01-00021.2002
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发表时间：
2002-01-01
影响因子：
5.3
通讯作者：
Regehr, WG
中科院分区：
文献类型：
--
作者：
Carter, AG;Vogt, KE;Regehr, WG
最近的证据表明，体内的钙储存和钙诱导的钙释放(CICR)提供了一个重要的钙来源，推动了中央突触的短期突触前可塑性。在这里，我们测试了CICR在急性大鼠海马和小脑脑片的六个兴奋性突触的短期突触前可塑性中的作用。用thapsigargin耗尽体内钙库和用ryanodine预防CICR对双脉冲易化、神经递质延迟释放或钙依赖的抑郁恢复没有影响。荧光钙测量也表明，这些药物对支持这些形式的短期突触前可塑性的残余钙信号没有影响。最后，虽然咖啡因导致浦肯野细胞体和树突的CICR，但它不会在平行的纤维输入到这些细胞中引发CICR。综上所述，这些结果表明，对于这里研究的兴奋性突触，内部钙储存和CICR在毫秒到秒的时间尺度上对突触前的短期可塑性没有贡献。相反，这种可塑性是由通过电压门控钙通道进入钙所产生的残余钙信号驱动的。
Recent evidence suggests that internal calcium stores and calcium-induced calcium release (CICR) provide an important source of calcium that drives short-term presynaptic plasticity at central synapses. Here we tested for the involvement of CICR in short-term presynaptic plasticity at six excitatory synapses in acute rat hippocampal and cerebellar brain slices. Depletion of internal calcium stores with thapsigargin and prevention of CICR with ryanodine have no effect on paired-pulse facilitation, delayed release of neurotransmitter, or calcium-dependent recovery from depression. Fluorometric calcium measurements also show that these drugs have no effect on the residual calcium signal that underlies these forms of short-term presynaptic plasticity. Finally, although caffeine causes CICR in Purkinje cell bodies and dendrites, it does not elicit CICR in parallel fiber inputs to these cells. Taken together, these results indicate that for the excitatory synapses studied here, internal calcium stores and CICR do not contribute to short-term presynaptic plasticity on the milliseconds-to-seconds time scale. Instead, this plasticity is driven by the residual calcium signal arising from calcium entry through voltage-gated calcium channels.