The sampling interval in the X-Y axis was adjusted so that at lea

The sampling interval in the X-Y axis was adjusted so that at least 100 cells were counted for each region of interest. Coefficient of error attributed to the sampling was calculated according to Gundersen & Jensen (1987). Errors = 0.10 were accepted. In Figs 4

and 6 data are expressed as percentage surviving cells and in Table 1 as percentage lost, with the intact hemisphere corresponding to 100% for each selleck products individual mouse. The average number of TH+ cells counted in the intact SN was 2698 ± 699.57 and the average in the VTA was 2645 ± 782.94. All data are expressed as mean ± SEM unless stated otherwise. All statistical analyses were conducted using the Statistical Package

Z-VAD-FMK clinical trial for the Social Sciences 17 (SPSS Inc.). A paired Student’s t-test was used to compare the number of midbrain TH+ neurons on the intact and 6-OHDA-injected side. Linear regression was performed on the densitometric values and cell counting in Fig. 4, the correlations between the performances in the different behavioural tests in Fig. 5 and the correlations between behavioural impairments and densitometric values and cell counts in Fig. 6. A one-way anova with a Tukey post hoc was performed on the behavioural data comparing subgroups of lesioned mice in Fig. 7. The long-term deficits observed in lesioned and intact animals (Fig. 8) were compared using a two-way anova using the generalised linear model and the Wald chi-square test, with main effects of group and time. A one-way anova with a Student–Newman–Keuls post hoc was performed Reverse transcriptase for all of the parameters described in Table 1, with all contrasts at least P < 0.05. The 6-OHDA injection was targeted at the mediolateral/anterior–posterior mid-point of the SN pars compacta, as illustrated

in a composite, horizontal TH-immunostained section in Fig. 2. The lesion caused in most cases a substantial loss of the A9 cells in the SN, while the A10 cells in the VTA were less affected. In the 40 mice included in the present study the total TH+ cell loss, in SN and VTA combined, ranged from −12 to −82% (mean, −58.5 ± 15.9%), which was highly significant compared to the intact hemisphere (t35 = −21.5; P < 0.0001). The loss of TH+ cells in the SN (−85.8 ± 15.7%; t35 = −31.2, P < 0.0001) was more severe than in VTA (−31.6 ± 18.6%; t35 = −9.8, P < 0.0001) when compared to the respective structures in the intact hemisphere. Representative examples of the extent of TH+ cell loss in animals with varying degrees of degeneration are illustrated in Fig. 3. As illustrated in the TH-stained sections in Fig. 3, the loss of TH+ cell bodies was accompanied by a substantial loss of TH+ innervation in the striatum.

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