Glutamate-mediated cytosolic calcium oscillations regulate a pulsatile prostaglandin release from cultured rat astrocytes. (Articolo in rivista)

Type
Label
  • Glutamate-mediated cytosolic calcium oscillations regulate a pulsatile prostaglandin release from cultured rat astrocytes. (Articolo in rivista) (literal)
Anno
  • 2003-01-01T00:00:00+01:00 (literal)
Alternative label
  • Zonta M., Sebelin A., Gobbo S., Fellin T., Pozzan T., Carmignoto G. (2003)
    Glutamate-mediated cytosolic calcium oscillations regulate a pulsatile prostaglandin release from cultured rat astrocytes.
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Zonta M., Sebelin A., Gobbo S., Fellin T., Pozzan T., Carmignoto G. (literal)
Pagina inizio
  • 407 (literal)
Pagina fine
  • 414 (literal)
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  • impact factor 4,352 (literal)
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  • 553 (literal)
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  • pubblicazione su rivista internazionale (literal)
Note
  • ISI Web of Science (WOS) (literal)
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  • Uni di PD, Dipartimento di Scienze Biomediche Sperimentali (literal)
Titolo
  • Glutamate-mediated cytosolic calcium oscillations regulate a pulsatile prostaglandin release from cultured rat astrocytes. (literal)
Abstract
  • The synaptic release of glutamate evokes in astrocytes periodic increases in [Ca2+]i, due to the activation of metabotropic glutamate receptors (mGluRs). The frequency of these [Ca2+]i oscillations is controlled by the level of neuronal activity, indicating that they represent a specific, frequency-coded signalling system of neuron-to-astrocyte communication. We recently found that neuronal activity-dependent [Ca2+]i oscillations in astrocytes are the main signal that regulates the coupling between neuronal activity and blood flow, the so-called functional hyperaemia. Prostaglandins play a major role in this fundamental phenomenon in brain function, but little is known about a possible link between [Ca2+]i oscillations and prostaglandin release from astrocytes. To investigate whether [Ca2+]i oscillations regulate the release of vasoactive prostaglandins, such as the potent vasodilator prostaglandin E2 (PGE2), from astrocytes, we plated wild-type human embryonic kidney (HEK)293 cells, which respond constitutively to PGE2 with [Ca2+]i elevations, onto cultured astrocytes, and used them as biosensors of prostaglandin release. After loading the astrocyte-HEK cell co-cultures with the calcium indicator Indo-1, confocal microscopy revealed that mGluR-mediated [Ca2+]i oscillations triggered spatially and temporally coordinated [Ca2+]i increases in the sensor cells. This response was absent in a clone of HEK cells that are unresponsive to PGE2, and recovered after transfection with the InsP3-linked prostanoid receptor EP1. We conclude that [Ca2+]i oscillations in astrocytes regulate prostaglandin releases that retain the oscillatory behaviour of the [Ca2+]i changes. This finely tuned release of PGE2 from astrocytes provides a coherent mechanistic background for the role of these glial cells in functional hyperaemia. (literal)
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