Figure 4.
Defects in corticostriatal short-term plasticity onto SPNs in Nrp2−/− mice. A, Schematic illustrating the experimental paradigm where SPNs were recorded in coronal striatal slices. A bipolar stimulating electrode was placed in the corpus callosum to stimulate corticostriatal fibers. B, Example of voltage responses to current steps for injection of an SPN. C, D, Representative examples of EPSPs measured in SPNs after a pair of electrical stimuli. ISIs: 20 ms in C; 100 ms in D. Responses of SPNs recorded in WT are represented in blue, and mutant in red. Note that in WT SPNs, there is a strong paired-pulse facilitation that is impaired in Nrp2−/−. E, Box plots representing the paired-pulse ratio of the responses at different ISIs (20, 40, 60, 80, 100, 120, and 200 ms) for the two genotypes. Responses are expressed as a ratio of the response to the first stimulus. F, Representative current-clamp traces showing corticostriatal EPSPs elicited by paired stimuli with increasing ISIs in WT mice (F1) and Nrp2−/− (F2). G, Summary graph of PPRs recorded from medium spiny neurons plotted against ISIs for cortical stimulation in WT (blue) and Nrp2−/− (red). Box plots represent the minimum, maximum interquartile range, the mean, and the median. Statistical analysis was made using unpaired t test (E) where ***p = 0.0009, 20 ms; ***p = 0.0010, 40 ms; ***p = 0.0002, 60 ms; *p = 0.0117, 80 ms; *p = 0.0391, 100 ms; **p = 0.0071, 120 ms; and *p = 0.0303, 200 ms comparison between WT and Nrp2−/−, and two-way ANOVA (G).