Calcium signals activated by arachidonic acid in embryonic chick ciliary ganglion neurons

Jessica Erriquez, Alessandra Gilardino, Paolo Ariano, Luca Munaron, Davide Lovisolo, Carla Distasi

Research output: Contribution to journalArticlepeer-review


Arachidonic acid (AA, 20:4) has been reported to modulate a variety of calcium-permeable ionic channels, both in the plasma membrane and in the endoplasmic reticulum. We have studied the effects of AA on calcium signaling in a well-characterized model of developing peripheral neurons, embryonic chick ciliary ganglion neurons in culture. When given at low non-micellar concentrations (5 μM), in the majority of cells AA directly activated a delayed and long-lasting increase in [Ca2+]i, involving both the cytoplasm and the nucleoplasm, that was completely reversed by abolition of extracellular calcium. Other fatty acids (FAs), either saturated like arachidic acid (20:0), or unsaturated like linoleic (18:2) and docosahexaenoic acid (22:6), shared its ability to activate calcium influx. This entry was not suppressed by voltage-dependent calcium channel inhibitors ω-conotoxin and nifedipine, by the voltage-independent calcium channel antagonist LOE-908, by pre-treatment with blockers of AA metabolic pathways or with pertussis toxin. The arachidonate-activated calcium pathway was permeable to Mn2+ and blocked by La3+, Gd3+ and Ni 2+. In a neuronal subpopulation, AA at the same concentration was also able to elicit calcium release from thapsigargin-sensitive intracellular stores; we provide evidence that cytochrome P450 epoxygenase is involved in this process.

Original languageEnglish
Pages (from-to)244-254
Number of pages11
Issue number5
Publication statusPublished - Nov 2005


  • Arachidonic acid
  • Calcium release
  • Chick embryo
  • Non-capacitative calcium entry

ASJC Scopus subject areas

  • Neuroscience(all)


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