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. 2001 Jan 16;98(3):1255–1260. doi: 10.1073/pnas.031374698

Figure 1.

Figure 1

Loss of the developmental increases in PPR in intrastriatal 6-OHDA-treated rats and D2KO mice. (A) The left traces are EPSCs elicited by paired stimuli (50-ms interpulse interval) recorded in neurons from different aged VEH-treated rats (upper traces, PD13; lower traces, PD26). The right traces are EPSCs recorded in neurons from different aged 6-OHDA-treated rats (upper traces, PD16; lower traces, PD26). (B) Summary plot of PPR across the early postnatal developmental period. Data obtained from VEH- (40 neurons in 19 rats) and 6-OHDA- (74 neurons in 28 rats) treated animals are expressed as open and solid circles, respectively. Number of cells recorded in VEH-treated rats at different ages was 4 at PD13, 5 at PD14, 3 at PD17, 8 at PD20, 5 at PD23, 4 at PD24, 4 at PD 25, 3 at PD26, and 4 at PD29. Number of cells recorded in 6-OHDA-treated rats at different ages was 4 at PD14, 3 at PD16, 4 at PD17, 4 at PD18, 7 at PD19, 7 at PD20, 5 at PD 21, 8 at PD22, 8 at PD23, 12 at PD24, 8 at PD25, and 4 at PD26. Two-way ANOVA analysis showed that PPR was significantly different between 6-OHDA-treated and VEH-treated rats (F = 65.6, df = 1/65, P < 0.0001) and dependent upon age (F = 2.79, df = 6/65, P < 0.05). (C) The extent of DA denervation was examined by performing TH immunostaining on 40-μm-thick brain sections after electrophysiological experiments were completed. (Left) VEH injection. (Right) 6-OHDA injection. (D) Left traces are EPSCs recorded in neurons from different aged WT mice (upper traces, PD12; lower traces, PD24). The right traces are EPSCs recorded from different aged D2KO mice (upper traces, PD15; lower traces, PD25). (E) Summary plot of PPR across the early postnatal developmental period. Data obtained from WT (89 neurons in 30 mice) and D2KO (80 neurons in 28 mice) animals are expressed as open and solid circles, respectively. Number of cells recorded in WT mice was 6 at PD12, 8 at PD13, 3 at PD14, 8 at PD15, 3 at PD16, 6 at PD18, 10 at PD19, 4 at PD20, 4 at PD21, 13 at PD22, 15 at PD23, 4 at PD24, and 5 at PD27. Number of cells recorded in D2KO mice was 13 at PD13, 5 at PD14, 5 at PD15, 6 at PD16, 9 at PD17, 7 at PD18, 12 at PD22, 9 at PD23, 7 at PD25, and 7 at PD27. Two-way ANOVA analysis showed that PPR was significantly different between WT and D2KO mice (F = 20.00, df = 1/99, P < 0.0001) and dependent upon age (F = 2.14, df = 7/99, P < 0.05). Further analysis with one-way ANOVA indicated no significant change in PPR during postnatal development in 6-OHDA-treated rats (F = 0.25, df = 6/40, P > 0.95) and D2KO mice (F = 0.83, df = 7/52, P > 0.84). However, there was a significant increase in PPR during postnatal development in VEH-treated rats (F = 3.35, df = 6/25, P < 0.05) and WT mice (F = 3.97, df = 7/53, P < 0.01).