FIGURE 3.

Prenatal LPS exposure increases the production of NO by astrocytes and the Panx1 channel-dependent release of ATP on offspring hippocampus. Representative images showing SR101 (red) and DAF-FM (green) staining by hippocampal astrocytes in acute slices from control offspring (A) or prenatally LPS-exposed offspring (B) of 4 months old. Insets of astrocytes were taken from the area depicted within the red squares in (A,B). (C) Averaged of DAF-FM signal fluorescence by astrocytes in acute slices from control offspring (white bar) or prenatally LPS-exposed offspring of 4 months old alone (black bars) or in combination with the following pharmacological agents: 100 μM gap19, 100 μM ¹⁰panx1 and 1 μM L-N6. ^∗p < 0.0001 versus LPS, one-way ANOVA Tukey’s post hoc test, mean ± S.E.M., n = 3. (D) Averaged data of ATP release by acute hippocampal slices from control offspring (white bar) or prenatally LPS-exposed offspring of 4 months old alone (black bars) or in combination with the following blockers: 100 μM gap19, 100 μM ¹⁰panx1 and 1 μM L-N6. ^∗p < 0.0001 versus LPS, ^#p < 0.0001 versus control, one-way ANOVA Tukey’s post hoc test, mean ± S.E.M., n = 3. Calibration bar = 85 μm.