期刊
BRAIN RESEARCH
卷 1503, 期 -, 页码 7-15出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2013.02.002
关键词
Vagal sensory nerves; Endoplasmic reticulum; Calcium; Nerve terminal; Store-operated calcium entry; Orai channel
资金
- NHLBI NIH HHS [R00 HL088520] Funding Source: Medline
Vagal sensory nerves innervate the majority of visceral organs (e.g., heart, lungs, GI tract, etc) and their activation is critical for defensive and regulatory reflexes. Intracellular Ca2+ is a key regulator of neuronal excitability and is largely controlled by the Ca2+ stores of the endoplasmic reticulum. In other cell types store-operated channels (SOC) have been shown to contribute to the homeostatic control of intracellular Ca2+. Here, using Ca2+ imaging, we have shown that ER depletion in vagal sensory neurons (using thapsigargin or caffeine) in the absence of extracellular Ca2+ evoked Ca2+ influx upon re-introduction of Ca2+ into the extracellular buffer. This store-operated Ca2+ entry (SOCE) was observed in approximately 25-40% of vagal neurons, equally distributed among nociceptive and non-nociceptive sensory subtypes. SOCE was blocked by Gd3+ but not by the Orai channel blocker SKF96365. We found Orai channel mRNA in extracts from whole vagal ganglia, but when using single cell RT-PCR analysis we found only 3 out of 34 neurons expressed Orai channel mRNA, indicating that Orai channel expression in the vagal ganglia was likely derived from non-neuronal cell types. Confocal microscopy of vagal neurons in 3 day cultures demonstrated rich ER tracker fluorescence throughout axonal and neurite structures and ER store depletion (thapsigargin) evoked Ca2+ transients from these structures. However, no SOCE could be detected in the axonal/neurite structures of vagal neurons. We conclude that SOCE occurs in vagal sensory neuronal cell bodies through non-Orai mechanisms but is absent at nerve terminals. (C) 2013 Elsevier B.V. All rights reserved.
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