Depletion of intracellular Ca 2/ gradually until E13, when the Ca 2/ rise almost disapstores induces a capacitative Ca 2/ influx in non-neural peared. This developmental profile correlated with the cells. It has been unknown whether the capacitative Ca 2/ influx occurs in the cells of nervous system
Ca2+ responses to acetylcholine and adenosine triphosphate in the otocyst of chick embryo
β Scribed by Nakaoka, Yoshikazu ;Yamashita, Masayuki
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 909 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0022-3034
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β¦ Synopsis
The action of acetylcholine and adenosine triphosphate (ATP) on cytoplasmic Ca2+ concentration ([Ca2+Ji) was studied in the otocyst epithelium of embryonic day 3 chicks with Ca2+-sensitive fluorescence measurements. Increases in [Ca2+li were evoked by the bath application of acetylcholine (1 pM or higher). The rise in [Ca2+Ii was due to the release of Ca2+ from intracellular Ca2+ stores, since the Ca2+ response occurred even in a Ca2+-free medium. The Ca2+ response to acetylcholine was mediated by muscarinic receptors. Atropine of 1 pM abolished the response to 10 pM acetylcholine; muscarine and carbamylcholine (100 pM each) evoked Ca2+ rises. Increases in [Ca2+li were also evoked by the bath application of ATP (10 pM or higher). The Ca2+ rise by ATP was evoked even in a Ca2+-free medium. Adenosine (500 p M ) did not cause any Ca2+ response. Suramin and reactive blue 2 (200 pM each) completely blocked the Ca2' response to 500 pM ATP. Uridine triphosphate (500 puM) caused comparable Ca2+ responses with those to 500 pM ATP. These results suggested the involvement of P2" purinoceptors. The potentiation of CaZ+ rise was observed when acetylcholine and ATP were co-applied at submaximal concentrations (10 p M a n d 100 pM, respectively). W e conclude that undifferentiated cells in the otocyst epithelium have Ca2+ mobilizing systems activated by acetylcholine and ATP.
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