Presynaptic T-Type Ca2+ Channels Modulate Dendrodendritic Mitral-Mitral and Mitral-Periglomerular Connections in Mouse Olfactory Bulb
Presynaptic T-Type Ca2+ Channels Modulate Dendrodendritic Mitral-Mitral and Mitral-Periglomerular Connections in Mouse Olfactory Bulb
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DOI：
10.1523/jneurosci.0905-14.2014
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发表时间：
2014-10-15
影响因子：
5.3
通讯作者：
Delaney, Kerry R.
中科院分区：
文献类型：
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作者：
Fekete, Adam;Johnston, Jamie;Delaney, Kerry R.
二尖瓣细胞在其远端顶丛树突上表达低压激活的Cav3.3通道（McKay等人，2006;约翰斯顿和Delaney，2010）。它们还释放Na+依赖性树突动作电位并从这些树突释放谷氨酸。在静息膜电位附近，在-65和-50 mV之间，Cav3.x通道是细胞质[Ca 2 +]的主要决定因素。在这项研究中，使用C57小鼠，我们提出的证据表明，阈下Cav3.x介导的Ca 2+内流调节动作电位诱发的递质释放，并直接驱动从远端簇树突的异步释放。用Z941对Cav3.x通道的突触前超极化和选择性阻断（Tringham等人，2012）降低二尖瓣-二尖瓣EPSP振幅，增加EPSP的变异系数，并增加配对脉冲比，与降低的发射器释放概率一致。超极化和Cav3.x通道阻断均降低簇状树突中的稳态胞质[Ca 2 +]，而不降低动作电位诱发的Ca 2+内流，表明背景[Ca 2 +]调节诱发的释放。我们证明，Cav 3. x介导的Ca 2+内流，即使是一个二尖瓣细胞在膜电位在-65和-50 mV之间，足以产生反馈抑制肾小球周围神经元。Cav3.x通道通过超极化失活增加复极化时T型Ca 2+内流，并增加反馈抑制，以产生二尖瓣-肾小球周围互易回路的阈下调制。
Mitral cells express low-voltage activated Cav3.3 channels on their distal apical tuft dendrites (McKay et al., 2006; Johnston and Delaney, 2010). They also discharge Na+-dependent dendritic action potentials and release glutamate from these dendrites. Around resting membrane potentials, between -65 and -50 mV, Cav3.x channels are a primary determinant of cytoplasmic [Ca2+]. In this study using C57 mice, we present evidence that subthreshold Cav3.x-mediated Ca2+ influx modulates action potential evoked transmitter release and directly drives asynchronous release from distal tuft dendrites. Presynaptic hyperpolarization and selective block of Cav3.x channels with Z941 (Tringham et al., 2012) reduce mitral-to-mitral EPSP amplitude, increase the coefficient of variation of EPSPs, and increase paired-pulse ratios, consistent with a reduced probability of transmitter release. Both hyperpolarization and Cav3.x channel blockade reduce steady-state cytoplasmic [Ca2+] in the tuft dendrite without reducing action potential evoked Ca2+ influx, suggesting that background [Ca2+] modulates evoked release. We demonstrate that Cav3.x-mediated Ca2+ influx from even one mitral cell at membrane potentials between -65 and -50 mV is sufficient to produce feedback inhibition from periglomerular neurons. Deinactivation of Cav3.x channels by hyperpolarization increases T-type Ca2+ influx upon repolarization and increases feedback inhibition to produce subthreshold modulation of the mitral-periglomerular reciprocal circuit.