BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Talks.cam//talks.cam.ac.uk//
X-WR-CALNAME:Talks.cam
BEGIN:VEVENT
SUMMARY:Electrophysiology of autocrine and paracrine NMDA receptor signall
 ing in invasive mouse pancreatic neuroendocrine tumour cells - Dr Hugh Rob
 inson\, PDN\, University of Cambridge
DTSTART:20170316T160000Z
DTEND:20170316T170000Z
UID:TALK70110@talks.cam.ac.uk
CONTACT:Maria Schacker
DESCRIPTION:N-methyl-D-aspartate receptor (NMDAR) activation is implicated
  in the\nmalignant progression of many cancer types\, as validated functio
 nally\nthrough the use of NMDAR antagonists. NMDAR-mediated calcium influx
 \nand its downstream signalling depend critically on the dynamics of\nmemb
 rane potential and ambient glutamate concentration. Here\, we have\nused l
 ow-noise whole-cell patch-clamp recording to investigate the\nelectrophysi
 ology of glutamate signalling in pancreatic neuroendocrine\ntumour (PanNET
 ) cells derived from a genetically-engineered mouse\nmodel (GEMM) of PanNE
 T\, in which NMDAR signalling promotes cancer\nprogression. Activating NMD
 ARs is shown to cause excitation and\nintracellular calcium elevation\, an
 d intracellular perfusion with\nphysiological levels of glutamate leads to
  a VGLUT-dependent autocrine\nNMDAR activation. Necrotic cells are shown t
 o release endogenous\ncytoplasmic glutamate\, producing intense NMDAR acti
 vation in nearby\ncells. Computational modelling\, based on these results\
 , predicts that\nNMDARs in cancer cells could be strongly activated in the
  tumour\nmicroenvironment by both autocrine glutamate release and necrosis
 .
LOCATION:Hodgkin Huxley Seminar Room\, Physiology Building\, Downing Site
END:VEVENT
END:VCALENDAR