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Fig. 1 | Cell & Bioscience

Fig. 1

From: Complement C1q-mediated microglial synaptic elimination by enhancing desialylation underlies sevoflurane-induced developmental neurotoxicity

Fig. 1

Cognitive dysfunction and synapse loss in the hippocampus of mice after neonatal sevoflurane exposures. A Scheme of neonatal mice receiving repeated sevoflurane and the MWM test. Neonatal mice were exposed to 3% sevoflurane on PNDs 6, 8, and 10, and then the memory and learning abilities were assessed using the MWM test on PNDs 31–36. B Tracking plots of mice. C Sevoflurane reduced the escape latency compared to the control group on PNDs 33–35, as well as the platform crossing times and times spent in the target quadrant. Swimming speed was similar between groups. n = 8. Unpaired t-test and two-way ANOVA. D Representative confocal microscopy images displaying the immunoreactivity of the presynaptic marker Vglut2 (green) and postsynaptic marker PSD95 (red) in the hippocampus. Scale bar = 5 μm. E The sevoflurane group showed decreased density of Vglut2 and PSD95. n = 6. Unpaired t-test. F Colocalization analysis showed that the density of synapses was lower in sevoflurane-treated mice. n = 6. Unpaired t-test. G Representative Western blot bands of Vglut2 and PSD95 in the two groups. (H) Quantification of Western blot showed that the expression of Vglut2 and PSD95 was decreased in sevoflurane-treated mice. n = 4. Unpaired t-test. I Representative Golgi-Cox staining images of dendritic spines in the hippocampus. Scale bar = 5 μm. J Quantification of the density of dendritic spines showed that the sevoflurane group had a lower spine density. n = 6. Unpaired t-test. Data are mean ± SEM. *P < 0.05, ** P < 0.01, *** P < 0.001. MWM, Morris water maze; PND, postnatal day

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