Espinosa Parrilla, Juan FranciscoMartínez Moreno, MartínGasull Casanova, XavierMahy Gehenne, Josette NicoleRodríguez Allué, Manuel José2015-02-202015-02-202015-12-121044-7431https://hdl.handle.net/2445/63186Under 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.39 p.application/pdfeng(c) Elsevier B.V., 2015MicrògliaCanals de calciSistema nerviós centralMalalties neurodegenerativesMicrogliaCalcium channelsCentral nervous systemNeurodegenerative Diseasesinfo:eu-repo/semantics/article6452552015-02-20info:eu-repo/semantics/openAccess25497271