Nonlinear regulation of unitary synaptic signals by CaV2.3 voltage-sensitive calcium channels located in dendritic spines
Nonlinear regulation of unitary synaptic signals by CaV2.3 voltage-sensitive calcium channels located in dendritic spines
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DOI：
10.1016/j.neuron.2006.12.017
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发表时间：
2007-01-18
期刊：
影响因子：
16.2
通讯作者：
Sabatini, Bernardo L.
中科院分区：
文献类型：
--
作者：
Bloodgood, Brenda L.;Sabatini, Bernardo L.
位于树突和棘上的电压敏感性钠（Na）和钙（Ca）通道在调节突触信号中的作用在很大程度上是未知的。在这里，我们使用2-光子谷氨酸解开刺激个人的脊椎，同时监测解开诱发的兴奋性突触后电位（uEPSP）和钙瞬变。我们发现，在急性小鼠海马切片的CA 1锥体神经元中，CaV2.3电压敏感性钙通道（VSCC）被发现选择性地在棘上，并在局部发挥作用，以抑制未老化诱发的钙瞬变和体细胞电位。这些作用是由一个调节环介导的，该调节环需要打开CaV2.3通道、电压门控Na通道、小电导Ca激活钾（SK）通道和NMDA受体。通过CaV2.3 VSCCS的Ca内流选择性地激活SK通道，揭示了脊柱内功能性Ca微结构域的存在。我们的研究结果表明，突触强度可以调制的机制，调节电压门控电导内的脊柱，但不改变突触谷氨酸受体的属性或数量。
The roles of voltage-sensitive sodium (Na) and calcium (Ca) channels located on dendrites and spines in regulating synaptic signals are largely unknown. Here we use 2-photon glutamate uncaging to stimulate individual spines while monitoring uncaging-evoked excitatory postsynaptic potentials (uEPSPs) and Ca transients. We find that, in CA1 pyramidal neurons in acute mouse hippocampal slices, CaV2.3 voltage-sensitive Ca channels (VSCCs) are found selectively on spines and act locally to dampen uncaging-evoked Ca transients and somatic potentials. These effects are mediated by a regulatory loop that requires opening of CaV2.3 channels, voltage-gated Na channels, small conductance Ca-activated potassium (SK) channels, and NMDA receptors. Ca influx through CaV2.3 VSCCS selectively activates SK channels, revealing the presence of functional Ca microdomains within the spine. Our results suggest that synaptic strength can be modulated by mechanisms that regulate voltage-gated conductances within the spine but do not alter the properties or numbers of synaptic glutamate receptors.