dMSN selectivity is reduced with neonatal dopaminergic lesion. A, Schematic representation of the positioning of Prl and Cg stimulation electrodes. B, Reconstruction of the position of the recorded dMSNs in lesioned mice. C, Representative traces showing responses of dMSN of lesioned animals to Prl and Cg stimulation. D, E, Intensity response curves of dMSN to Prl (D) and Cg (E) stimulation. For Prl, the average cells' response is shown. For Cg/M2, each line is a cell, and the number of responding neurons/recorded neurons is shown. There are no differences in the response to Prl stimulation (D, two-way repeated-measures ANOVA, nonsignificant interaction: F₍₇₁₈₉₎ = 0.9441, p = 0.4737). In lesioned animals, dMSNs are more responsive to Cg inputs (E, 400 µA: Mann–Whitney test, U = 50.5, **p = 0.0080). F, Minimal cortical stimulation current (threshold) needed to induce dMSN response to Cg/M2 stimulation is lower in lesioned animals (Prl: Mann–Whitney test, U = 83, p = 0.4656; Cg/M2: Mann–Whitney test, U = 12.5, *p = 0.0398). G, Prl input selectivity, calculated as the difference in Prl and Cg/M2 responses, is reduced in lesioned mice (unpaired t test: t₍₂₆₎ = 2.064, *p = 0.0492). H, Latency of dMSN response to Prl and Cg/M2 stimulation is shorter in lesioned animals, and latencies are longer for Cg/M2 than for Prl (mixed-effects analysis: significant effect of lesion, F_(1,27) = 6.439, *p = 0.0173; significant effect of cortical region, F_(1,13) = 4.982, *p = 0.0438). I, Spontaneous activity of dMSN did not differ between groups (Mann–Whitney test, U = 95, p = 0.5936). F–I, Each black dot represents an individual cell. Data are mean ± SEM (G,H) or median and interquartile range (F,I).