Tat-induced microglial phagocytosis of axons is partially dependent on phosphatidylserine signaling. In order to determine if Tat-induced BV-2 cell phagocytosis of axons was phosphatidylserine dependent, we blocked phosphatidylserine exposure with AnnexinV. (A) Microfluidic chambers are shown before treatment. (B) The addition of AnnexinV protected the axon field from Tat-treated BV-2 cells in microfluidic chambers. (C) Using qRT-PCR, we measured the expression of the phosphatidylserine receptor BA1 in monoculture BV-2 cells exposed to Tat or saline for 12 hours ± LRRK2i. Tat treatment increased BA1 expression, although not significantly. LRRK2i significantly decreased BA1 expression in Tat treated BV-2 cells (*P <0.05, one way ANOVA, Newman-Keuls post-test). ANOVA, analysis of variance; LRRK2i, leucine-rich repeat kinase 2 inhibitor; Tat, trans activator of transcription.