Extracellular H+ induces Ca2+ signals in respiratory chemoreceptors of zebrafish
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- 作者：Sara J. Abdallah ; Michael G. Jonz…
- 关键词：Calcium ; Hypercapnia ; Neuroepithelial cells ; pH ; Chemoreceptor ; Zebrafish
- 刊名：Pflügers Archiv - European Journal of Physiology
- 出版年：2015
- 出版时间：February 2015
- 年：2015
- 卷：467
- 期：2
- 页码：399-413
- 全文大小：995 KB
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15. Gilmour KM & Perry S - 作者单位：Sara J. Abdallah (1)
Michael G. Jonz (1)
Steve F. Perry (1)
1. Department of Biology, University of Ottawa, 30 Marie Curie Pvt., Ottawa, ON, K1N 6N5, Canada - 刊物主题：Human Physiology;
- 出版者：Springer Berlin Heidelberg
- ISSN：1432-2013
文摘
Neuroepithelial cells (NECs) of the fish gill are respiratory chemoreceptors that detect changes in O2 and CO2/H+ and are homologous to type I cells of the mammalian carotid body. In zebrafish (Danio rerio), stimulation of NECs by hypoxia or hypercapnia initiates inhibition of K+ channels and subsequent membrane depolarisation. The goal of the present study was to further elucidate, in zebrafish NECs, the signalling pathways that underlie CO2/H+ sensing and generate intracellular Ca2+ ([Ca2+]i) signals. Breathing frequency was elevated maximally in fish exposed to 5?% CO2 (~37.5?mmHg). Measurement of [Ca2+]i in isolated NECs using Fura-2 imaging indicated that [Ca2+]i increased in response to acidic hypercapnia (5?% CO2, pH?6.6) and isocapnic acidosis (normocapnia, pH?6.6), but not to isohydric hypercapnia (5?% CO2, pH?7.6). Measurement of intracellular pH (pHi) using BCECF demonstrated a rapid decrease in pHi in response to acidic and isohydric hypercapnia, while isocapnic acidosis produced a smaller change in pHi. Intracellular acidification was reduced by the carbonic anhydrase inhibitor, acetazolamide, without affecting [Ca2+]i responses. Moreover, intracellular acidification using acetate (at constant extracellular pH) was without effect on [Ca2+]i. The acid-induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+ and was unaffected by Ca2+ channel blockers (Cd2+, Ni2+ or nifedipine). The results of this study demonstrate that, unlike type I cells, extracellular H+ is critical to the hypercapnia-induced increase in [Ca2+]i in NECs. The increase in [Ca2+]i occurs independently of pHi and appears to originate primarily from Ca2+ derived from intracellular stores.