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Signaling pathways to resilience or dysfunction in the brain

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

RESEARCH SUMMARY : In central neurons, Ca2+ entry through the NMDA -type glutamate receptor (NMDAR) is a major source of synaptically-evoked Ca2+ transients and directly affects neuronal survival/death: while too much NMDAR activity is harmful, so is too little (Hardingham and Bading, 2003; Papadia and Hardingham, 2007). Understanding the mechanisms behind this dichotomous signalling is an area of molecular neuroscience with direct clinical implications. The research of my group focuses on understanding the signalling events that are triggered by NMDAR activity, and their impact on neuronal survival and death, and comprise three main themes.

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