Premium
Intercellular Ca 2+ waves in rat hippocampal slice and dissociated glial–neuron cultures mediated by nitric oxide
Author(s) -
Willmott Nicholas J.,
Wong Kay,
Strong Anthony J.
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02359-0
Subject(s) - nitric oxide , intracellular , neuron , hippocampal formation , chemistry , biophysics , neuroglia , microbiology and biotechnology , neuroscience , biology , biochemistry , central nervous system , organic chemistry
Nitric oxide (NO) may participate in cell–cell communication in the brain by generating intercellular Ca 2+ waves. In hippocampal organotypic and dissociated glial–neuron (>80% glia) cultures local applications of aqueous NO induced slowly propagating intercellular Ca 2+ waves. In glial cultures, Ca 2+ waves and Mn 2+ quench of cytosolic fura‐2 fluorescence mediated by NO were inhibited by nicardipine, indicating that NO induces Ca 2+ influx in glia which is dihydropyridine‐sensitive. As NO treatments also depolarised the plasma membrane potential of glia, the nicardipine‐sensitive Ca 2+ influx might be due to the activation of dihydropyridine‐sensitive L‐type Ca 2+ channels. Both nicardipine‐sensitive intercellular Ca 2+ waves and propagating cell depolarisation induced by mechanical stress of individual glia were inhibited by pretreating cultures with either an NO scavenger or N G ‐methyl‐ L ‐arginine. Results demonstrate that NO can induce Ca 2+ waves in hippocampal slice cultures, and that Ca 2+ influx coupled to NO‐mediated membrane depolarisation might assist in fashioning their spatio‐temporal dynamics.