Electrophysiology of autocrine and paracrine NMDA receptor signalling in invasive mouse pancreatic neuroendocrine tumour cells

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• Dr Hugh Robinson, PDN, University of Cambridge
• Thursday 16 March 2017, 16:00-17:00
• Hodgkin Huxley Seminar Room, Physiology Building, Downing Site.

If you have a question about this talk, please contact Maria Schacker.

N-methyl-D-aspartate receptor (NMDAR) activation is implicated in the malignant progression of many cancer types, as validated functionally through the use of NMDAR antagonists. NMDAR -mediated calcium influx and its downstream signalling depend critically on the dynamics of membrane potential and ambient glutamate concentration. Here, we have used low-noise whole-cell patch-clamp recording to investigate the electrophysiology of glutamate signalling in pancreatic neuroendocrine tumour (PanNET) cells derived from a genetically-engineered mouse model (GEMM) of PanNET, in which NMDAR signalling promotes cancer progression. Activating NMDA Rs is shown to cause excitation and intracellular calcium elevation, and intracellular perfusion with physiological levels of glutamate leads to a VGLUT -dependent autocrine NMDAR activation. Necrotic cells are shown to release endogenous cytoplasmic glutamate, producing intense NMDAR activation in nearby cells. Computational modelling, based on these results, predicts that NMDA Rs in cancer cells could be strongly activated in the tumour microenvironment by both autocrine glutamate release and necrosis.

This talk is part of the Foster Talks series.

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