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sch is a dopamine d2 receptor antagonist and is commonly used to induce the parkinsonian phenotype in animals. when applied to mice, sch (0.2mg/kg) reduces spontaneous locomotion during the first 30min and induces a loss of coordination and deficits in the bar test (see above) (fig. 6g ) (is group median equal to the theoretical median of 20s: p=0.0005, one sample wilcoxon test). the pharmacological deficit was not rescued by optogenetic activation of vglut2-ppn neurons (fig. 6g, h and s3f) (comparison of time spent moving during laser-on: two-way rm anova, laser f(1, 9)=16.51, p=0.0030. fraction of successful trials: p=0.2537, two-tailed, paired t-test).
having demonstrated the robust response of the vglut2-ppn neurons to optogenetic stimulation in both the absence and presence of dopamine receptor blockade we went on to investigate whether vglut2-ppn activation was effective at restoring locomotion in pd-like models. in order to induce a pd-like phenotype we employed two different pharmacological strategies. the first was acute administration of the dopamine receptor antagonist haloperidol (1mg/kg) followed by a 4-hour washout. the second involved the continuous administration of the dopamine receptor antagonist sch 23390 (0.1mg/kg) via osmotic pump throughout the experiment. in both cases we observed a decrease in locomotion after a 30min period of acute drug administration that was well-reflected in the bar test (fig. 6i, j ). optogenetic activation of vglut2-ppn neurons rescued the impaired motor function in both haloperidol- (fig. 7a) (two-way rm anova, laser f(1, 12)=12.41, p=0.0040. fraction of successful trials: p=0.0309, two-tailed, paired t-test. latency: wilcoxon matched-pairs, two-tailed, p=0.0035, w=34) and sch-treated mice (fig. 7b) (two-way rm anova, laser f(1, 9)=19.08, p=0.0045.0310, two-tailed, paired t-test; t=2.782, df=9). p=0.0056, one-tailed paired t-test, laser-on-trials sal+cno
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