ROCK/Cdc42-mediated microglial motility and gliapse formation lead to phagocytosis of degenerating dopaminergic neurons in vivo

Carlos Barcia*, Carmen María Ros, Valentina Annese, María Angeles Carrillo De Sauvage, Francisco Ros-Bernal, Aurora Gómez, José Enrique Yuste, Carmen María Campuzano, Vicente De Pablos, Emiliano Fernandez-Villalba, María Trinidad Herrero

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

89 Citations (Scopus)

Abstract

The role of microglial motility in the context of adult neurodegeneration is poorly understood. In the present work, we investigated the microanatomical details of microglia-neuron interactions in an experimental mouse model of Parkinson's disease following the intraperitoneal injection of MPTP. The specific intoxication of dopaminergic neurons induces the cellular polarization of microglia, leading to the formation of body-to-body neuron-glia contacts, called gliapses, which precede neuron elimination. Inhibiting ROCK/Cdc42-mediated microglial motility in vivo blocks the activating features of microglia, such as increased cell size and number of filopodia and diminishes their phagocyting/secreting domains, as the reduction of the Golgi apparatus and the number of microglia-neuron contacts has shown. High-resolution confocal images and three-dimensional rendering demonstrate that microglia engulf entire neurons at one-to-one ratio, and the microglial cell body participates in the formation of the phagocytic cup, engulfing and eliminating neurons in areas of dopaminergic degeneration in adult mammals.

Original languageEnglish
Article number809
JournalScientific Reports
Volume2
DOIs
Publication statusPublished - 2012

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