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The L-type voltage-gated calcium channel modulates microglial pro-inflammatory activity

By J.F. Espinosa-Parrilla, M. Martínez-Moreno, Xavier Gasull Casanova, Josette Nicole Mahy Gehenne and Manuel José Rodríguez Allué

Abstract

Under pathological conditions, microglia, the resident CNS immune cells, become reactive and release pro-inflammatory cytokines and neurotoxic factors. We investigated whether this phenotypic switch includes changes in the expression of the L-type voltage-gated calcium channel (VGCC) in a rat model of N-methyl-d-aspartate-induced hippocampal neurodegeneration. Double immunohistochemistry and confocal microscopy evidenced that activated microglia express the L-type VGCC. We then analyzed whether BV2 microglia express functional L-type VGCC, and investigated the latter's role in microglial cytokine release and phagocytic capacity. Activated BV2 microglia express the CaV1.2 and CaV1.3 subunits of the L-type VGCC determined by reverse transcription-polymerase chain reaction, Western blot and immunocytochemistry. Depolarization with KCl induced a Ca2+ entry facilitated by Bay k8644 and partially blocked with nifedipine, which also reduced TNF-α and NO release by 40%. However, no nifedipine effect on BV2 microglia viability or phagocytic capacity was observed. Our results suggest that in CNS inflammatory processes, the L-type VGCC plays a specific role in the control of microglial secretory activity

Topics: Micròglia, Canals de calci, Sistema nerviós central, Malalties neurodegeneratives, Microglia, Calcium channels, Central nervous system, Neurodegenerative Diseases
Publisher: Elsevier B.V.
Year: 2015
DOI identifier: 10.1016/j.mcn.2014.12.004
OAI identifier: oai:diposit.ub.edu:2445/63186
Journal:

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