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. 2019 Nov 4;27(5):1588–1603. doi: 10.1038/s41418-019-0442-2

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© The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare 2019

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Fig. 2 — Levels of expression of glutamate receptors and massive accumulation of glycosylceramides are not responsible for increased sensitivity to glutamate in gba1^+/− and gba1^−/− neurons. a Expression of the glutamate receptors Grik2 and Grin2b in gba1^+/+, gba1^+/−, and gba1^−/− mice brains was measured at the mRNA level by qPCR (shown as scatter plot, mean ± SEM, n = 3 brains per genotype). These data show that Grik2 mRNA was slightly higher in gba1^+/− compared with the other genotypes, while Grin2b mRNA levels were decreased in gba1^+/− and gba1^−/− compared with gba1^+/+, showing that the increased glutamate sensitivity is not attributable to increased glutamate receptor expression (One-way Anova, post-hoc Bonferroni, **p < 0.01). b Protein expression of the glutamate receptors Grik2 and Grin2b in gba1^+/+, gba1^+/−, and gba1^−/− mice brains were measured by western blot (shown as scatter plot, mean ± SEM, n = 4–5 brains per genotype). These data show that the expression of these receptors was unchanged at the protein level (One-way Anova, post-hoc Bonferroni). c–m Analysis of lipidomics performed by mass spectrometry on lipids extracted from gba1^+/+, gba1^+/−, and gba1^−/− brains (n = 3 brains per genotype, data represented as scatter plot and mean ± SEM). Glycosylceramide (d18:1) levels were increased in gba1^−/− but not in gba1^+/+ and gba1^+/− brains (One-way Anova, post-hoc Bonferroni, ***p < 0.001) (c), suggesting that the enzyme activity produced by a single copy of GBA1 gene is sufficient to avoid substrate accumulation. Curiously, glycosylceramide (d18:0) levels were unchanged (d), as well as Cer, PC, lyso-PC, SM (e–h), while PE and PS are significantly changed in the disease models compared with wild-type brains (i–l)