Fig 2: VGLUT2 Is a Key Factor of Synaptic [Pi] Homeostasis during Development(A) Immunoblots (representative of 3–5 mice) show the expression of VGLUT1–3, synaptophysin (SyPh) and SV2A, GAPDH, and NaPi transporters PiT1 and 2 in murine synaptosomal preparations from developing (E18, postnatal day 3 [P3], and P5) or adult (P90) wild-type mice (left) or from E18 genotypes of the VGLUT2 mouse strains (right).(B) Pi content of E18 synaptosomes obtained from the VGLUT2-/- strain was drastically reduced in the absence of VGLUTs.(C) (Left) Normalized data from the experiments displayed in (B) show a genotype-specific decline of Pi uptake. (Right) Normalized data from (B) present the RB-mediated decrease in cytosolic Pi for each genotype as % of the control condition. In the absence of Pi, VGLUT activity restores Pi loss, a process inhibited by RB. No restoration of lost Pi takes place in the absence of any VGLUT, and RB has no effect.Values represent pmol [Pi]/µg of protein for each genotype (B) or % of the control condition (no Pi offered; C). Data are the mean ± SEM from at least 6 mice per genotype. Significance toward: (1) no Pi added; (5) VGLUT2 KO control; (6) VGLUT2 WT; and (7) VGLUT2 Het.