FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration

Ramón Martínez-Mármol, Bruna Barneda-Zahonero, David Soto, Rosa Maria Andrés, Elena Coccia, Xavier Gasull, Laura Planells-Ferrer, Rana S. Moubarak, Eduardo Soriano, Joan X. Comella

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6 Citations (Scopus)

Abstract

© 2016 The Author(s). Caspases have recently emerged as key regulators of axonal pruning and degeneration and of long-term depression (LTD), a long-lasting form of synaptic plasticity. However, the mechanism underlying these functions remains unclear. In this context, XIAP has been shown to modulate these processes. The neuron-specific form of FAIM protein (FAIM-L) is a death receptor antagonist that stabilizes XIAP protein levels, thus preventing death receptor-induced neuronal apoptosis. Here we show that FAIM-L modulates synaptic transmission, prevents chemical-LTD induction in hippocampal neurons, and thwarts axon degeneration after nerve growth factor (NGF) withdrawal. Additionally, we demonstrate that the participation of FAIM-L in these two processes is dependent on its capacity to stabilize XIAP protein levels. Our data reveal FAIM-L as a regulator of axonal degeneration and synaptic plasticity.
Original languageEnglish
Article number35775
JournalScientific Reports
Volume6
DOIs
Publication statusPublished - 21 Oct 2016

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    Martínez-Mármol, R., Barneda-Zahonero, B., Soto, D., Andrés, R. M., Coccia, E., Gasull, X., Planells-Ferrer, L., Moubarak, R. S., Soriano, E., & Comella, J. X. (2016). FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration. Scientific Reports, 6, [35775]. https://doi.org/10.1038/srep35775