Amplification of odor-induced Ca(2+) transients by store-operated Ca(2+) release and its role in olfactory signal transduction.
Amplification of odor-induced Ca(2+) transients by store-operated Ca(2+) release and its role in olfactory signal transduction.
复制标题
通过存储操作的 Ca(2) 释放放大气味诱导的 Ca(2) 瞬变及其在嗅觉信号转导中的作用。
DOI：
10.1152/jn.2000.83.1.501
复制
发表时间：
2000
影响因子：
2.5
通讯作者：
Greer,CA
中科院分区：
文献类型：
--
作者：
Zufall,F;Leinders-Zufall,T;Greer,CA
在脊椎动物嗅觉感受器神经元中，钙离子的一个重要作用是将气味诱导的兴奋与负责调节嗅觉敏感性的细胞内反馈通路连接起来，但细胞内钙离子储存在这一过程中的作用尚不清楚。利用共聚焦钙成像和穿孔斑片记录，我们发现火蜥蜴喙含有一个可释放的钙离子池，可被SERCA抑制剂thapsigargin和ryanodine受体激动剂咖啡因静息释放。Ca~(2+)的储存在空间上是受限的；排空会在树突和胞体中产生分区的Ca~(2+)释放和容量性的Ca~(2+)进入，但不会在纤毛中产生，纤毛是气味传递的场所。我们耗尽存储器以表明气味刺激引起存储器依赖的钙离子动员。气味诱导的这种钙离子释放似乎不是产生即时电生理反应所必需的，也不是对嗅觉纤毛中的钙瞬变有显著贡献。相反，它对于放大树突和胞体中钙瞬变的幅度和持续时间是重要的，因此对于气味诱导的钙波从纤毛传播到胞体是必要的。我们证明这一扩增过程依赖于钙离子诱导的钙离子释放。结果表明，气味刺激Orns可以引起细胞内钙离子的动员，而不会对受体电位产生直接影响。气味诱导的、依赖于储存的钙离子动员可能是反馈途径的一部分，通过该途径，信息从ORN的远端树突转移到其胞体。
A critical role of Ca2+in vertebrate olfactory receptor neurons (ORNs) is to couple odor-induced excitation to intracellular feedback pathways that are responsible for the regulation of the sensitivity of the sense of smell, but the role of intracellular Ca2+stores in this process remains unclear. Using confocal Ca2+imaging and perforated patch recording, we show that salamander ORNs contain a releasable pool of Ca2+that can be discharged at rest by the SERCA inhibitor thapsigargin and the ryanodine receptor agonist caffeine. The Ca2+stores are spatially restricted; emptying produces compartmentalized Ca2+release and capacitative-like Ca2+entry in the dendrite and soma but not in the cilia, the site of odor transduction. We deplete the stores to show that odor stimulation causes store-dependent Ca2+mobilization. This odor-induced Ca2+release does not seem to be necessary for generation of an immediate electrophysiological response, nor does it contribute significantly to the Ca2+transients in the olfactory cilia. Rather, it is important for amplifying the magnitude and duration of Ca2+transients in the dendrite and soma and is thus necessary for the spread of an odor-induced Ca2+wave from the cilia to the soma. We show that this amplification process depends on Ca2+-induced Ca2+release. The results indicate that stimulation of ORNs with odorants can produce Ca2+mobilization from intracellular stores without an immediate effect on the receptor potential. Odor-induced, store-dependent Ca2+mobilization may be part of a feedback pathway by which information is transferred from the distal dendrite of an ORN to its soma.