Glutamate-mediated overexpression of CD38 in astrocytes cultured with neurones

Santina Bruzzone, Claudia Verderio, Ursula Schenk, Ernesto Fedele, Elena Zocchi, Michela Matteolit, Antonio De Flora

Research output: Contribution to journalArticlepeer-review


Recently, a new system of astrocyte-neurone glutamatergic signalling has been identified. It is started in astrocytes by ectocellular, CD38-catalysed conversion of NAD+ to the calcium mobilizer cyclic ADP-ribose (cADPR). This is then pumped by CD38 itself into the cytosol where the resulting free intracellular Ca2+ concentration [Ca 2+]i transients elicit an increased release of glutamate, which can induce an enhanced Ca2+ response in neighbouring neurones. Here, we demonstrate that co-culture of either cortical or hippocampal astrocytes with neurones results in a significant overexpression of astrocyte CD38 both on the plasma membrane and intracellularly. The causal role of neurone-released glutamate in inducing overexpression of astrocyte CD38 is demonstrated by two observations: first, in the absence of neurones, induction of CD38 in pure astrocyte cultures can be obtained with glutamate and second, it can be prevented in co-cultures by glutamate receptor antagonists. The neuronal glutamate-mediated effect of neurones on astrocyte CD38 expression is paralleled by increased intracellular cADPR and [Ca2+]i levels, both findings indicating functionality of overexpressed CD38. These results reveal a new neurone-to-astrocyte glutamatergic signalling based on the CD38/cADPR system, which affects the [Ca2+]i in both cell types, adding further complexity to the bi-directional patterns of communication between astrocytes and neurones.

Original languageEnglish
Pages (from-to)264-272
Number of pages9
JournalJournal of Neurochemistry
Issue number1
Publication statusPublished - Apr 2004


  • Astrocytes
  • CD38
  • Cyclic ADP-ribose
  • Glutamate
  • Intracellular calcium
  • Neurones

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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