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Glutamate‐mediated overexpression of CD38 in astrocytes cultured with neurones

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 [Ca2+]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.