Ca2+-induced Ca2+ release mediates a slow post-spike hyperpolarization in rabbit vagal afferent neurons.
Ca2+-induced Ca2+ release mediates a slow post-spike hyperpolarization in rabbit vagal afferent neurons.
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DOI：
10.1152/jn.1998.79.2.688
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发表时间：
1998-02
影响因子：
2.5
通讯作者：
K. Moore;A. Cohen;J. Kao;D. Weinreich
中科院分区：
文献类型：
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作者：
K. Moore;A. Cohen;J. Kao;D. Weinreich
使用微荧光钙测量结合标准细胞内电流和电压钳记录技术，研究了急性解离的成年兔瘤神经元中Ca2+诱导的Ca2+释放（CICR）和Ca2+依赖的慢峰后超极化（AHPslow）之间的关系。用ap诱导的瞬时[Ca2+]i （DeltaCat）升高的幅度来监测CICR。在1 ~ 16 APs范围内，δ tacat的大小与AHPslow电流的大小密切相关（r = 0.985）。功能性CICR阻滞剂，ryanodine (10 nM), thapsigargin (100 nM), 2,5-二（t-丁基）对苯二酚（10 nM）或cyclopiazonic acid (10 nM)，选择性地降低AHPslow的峰幅bb0 /=91%。在5个神经元中，DeltaCat和AHPslow的同时记录显示，这两种反应同时被阻断。这些发现表明，CICR是兔结节神经元产生AHPslow的必要条件。DeltaCat的上升和衰减明显快于AHPslow。这种时间差异表明Ca2+激活AHPslow可能需要额外的信号转导步骤。
The relation between Ca2+-induced Ca2+ release (CICR) elicited by action potentials (APs) and a Ca2+-dependent slow post-spike hyperpolarization (AHPslow) in acutely dissociated adult rabbit nodose neurons was studied using microfluorimetric calcium measurements in conjunction with standard intracellular current- and voltage-clamp recording techniques. The magnitude of the AP-induced transient increase in [Ca2+]i (DeltaCat) was used to monitor CICR. There was a close correlation between the magnitude of the DeltaCat and the AHPslow current over the range of 1-16 APs (r = 0.985). Functional CICR blockers, ryanodine (10 muM), thapsigargin (100 nM), 2,5-di(t-butyl)hydroquinone (10 muM) or cyclopiazonic acid (10 muM), selectively reduced the peak amplitude of the AHPslow >/=91%. In five neurons, simultaneous recordings of the DeltaCat and the AHPslow revealed that both responses were blocked in parallel. These findings indicate that CICR is necessary for the generation of the AHPslow in rabbit nodose neurons. The DeltaCat rises and decays significantly faster than the AHPslow. This temporal disparity suggests that activation of the AHPslow by Ca2+ may require additional signal transduction steps.