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Calcium signaling in the choroid plexus epithelium (1097.11)
Author(s) -
Longden Thomas,
Bonev Adrian,
Nelson Mark
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1097.11
Subject(s) - choroid plexus , extracellular , endoplasmic reticulum , microbiology and biotechnology , calcium signaling , intracellular , calcium , chemistry , calcium in biology , biology , neuroscience , central nervous system , organic chemistry
Choroid plexus epithelial cells (ECs) express a diverse array of pumps and ion channels that facilitate the production of cerebrospinal fluid in the brain ventricles. Our understanding of the molecular players involved in EC function is advancing, but to date little is known about EC calcium (Ca 2+ ) signaling. We thus sought to determine the nature of Ca 2+ signaling in native preparations of rat choroid plexus loaded with the Ca 2+ indicator Fluo‐4, using high speed confocal imaging of intracellular Ca 2+ events. We observed three major forms of Ca 2+ events in ECs: 1) Uni‐ or multicellular propagating waves. 2) Brief, localized, high amplitude events reminiscent of IP 3 ‐mediated Ca 2+ release in endothelial cells, which we term Ca 2+ plexars. 1 3) Low amplitude quantal events reminiscent of TRPV4 sparklets in endothelial cells. 2 Ca 2+ activity in ECs was dependent on extracellular Ca 2+ , as its removal abolished all signals. Similarly, blockade of the sarco/endoplasmic reticulum ATPase terminated EC Ca 2+ signaling. At some sites, Ca 2+ plexars initiated sparklet activity. We conclude that Ca 2+ signaling in choroid plexus ECs is dependent on extracellular Ca 2+ entry, which causes the release of Ca 2+ from intracellular stores. Stores‐mediated plexar events also couple to sparklet events and may lead to regenerative Ca 2+ release. 1. Ledoux et al. (2008) PNAS 9: 1397‐1403 2. Sonkusare et al. (2012) Science 336 6081: 597‐601 Grant Funding Source : Supported by National Institutes of Health and the American Heart Association.