Mechanism Underlying the ATP‐Induced Increase in the Cytosolic Ca2+ Concentration in Chick Ciliary Ganglion Neurons

Masaru Sorimachi, Yumiko Abe, Katsutoshi Furukawa, Norio Akaike

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


Abstract: We examined the mechanism underlying the ATP‐induced increase in the cytosolic Ca2+ concentration ([Ca]in) in acutely isolated chick ciliary ganglion neurons, using fura‐2 microfluorometry. The ATP‐induced increase in [Ca]in was dependent on external Ca2+, was blocked in a dose‐dependent manner by reactive blue 2, and was substantially inhibited by both L‐ and N‐type Ca2+ channel blockers. ATP was effective in increasing [Ca]in in the presence of a desensitizing concentration of nicotine (100 µM), and simultaneous addition of maximal doses of ATP and nicotine caused an additive increase in [Ca]in, suggesting that ATP acts on a site distinct from nicotinic acetylcholine receptors. ATP also increased the cytosolic Na+ concentration as determined by sodium‐binding benzofuran isophthalate microfluorometry. These results suggest that ATP increases Na+ influx through P2 purinoceptor‐associated channels resulting in membrane depolarization, which in turn increases Ca2+ influx through voltage‐dependent Ca2+ channels. However, ATP still caused a small increase in [Ca]in under Na+‐free conditions, and this [Ca]in increase was little affected by Ca2+ channel blockers. ATP also increased Mn2+ influx under Na+‐free conditions, as indicated by quenching of fura‐2 fluorescence. These results suggest that nonselective cationic channels activated by ATP are permeable not only to Ca2+ but also to Mn2+, in addition to monovalent cations.

Original languageEnglish
Pages (from-to)1169-1174
Number of pages6
JournalJournal of Neurochemistry
Issue number3
Publication statusPublished - 1995 Mar


  • ATP
  • Ciliary ganglion cells
  • Cytosolic free Na
  • Fura‐2 microfluorometry
  • Nicotine
  • Reactive blue 2

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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