Journal
NEUROREPORT
Volume 12, Issue 9, Pages 2017-2020Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200107030-00046
Keywords
2-aminoethoxydiphenyl borate; calcium; fura-2; Gd3+; Ni2+; orexin; orexin receptor
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We have investigated Ca2+ release and receptor- and store-operated Ca2+ influxes in Chinese hamster ovary-ill cells expressing human OX1 orexin receptor. Receptor-operated Ca2+ influx-response to 3 nM orexin-A was not affected by Gd3+ or 2-APB (2-aminoethoxydiphenyl borate), but was inhibited by Ni2+. Store-operated Ca2+ influx was blocked by Ni2+. Gd3+ and 2-APB, whereas the thapsigargin-induced release was unaffected. 2-APB did not block inositol-1,4,5-trisphosphate-dependent Ca2+ release in these cells. Thus, low concentrations of orexin-A cause activation of two Ca2+ influxes in the cells: primarily, a receptor-operated Ca2+ influx, and secondarily, a store-depletion activated Ca2+ influx, which is subsequent to receptor-activated Ca2+ influx and the therewith-caused IS production. The results show that these two rely on different molecular entities. NeuroReport 12:2017-2020 (C) 2001 Lippincott Williams & Wilkins.
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