Extended Data Fig. 5: Assessment of dopamine axon GCaMP6s and striatal RdLight1 dynamics in RIM cKO^DA mice.

a, Schematic for assessment of fluorescence of GCaMP6s expressed in striatal dopamine axons and RdLight1 expressed in striatal neurons. b,c, Example traces (b) and cross-correlation (c) of GCaMP6s and RdLight1 signals, RIM control 4 mice, RIM cKO^DA 4. d,e, Individual (event heatmaps, top) and average (bottom) time courses of GCaMP6s (d) and RdLight1 (e) fluorescence aligned to the light flash (dashed line). Event heatmaps in d,e were sorted by the peak amplitude in d, RIM control 204 events from 4 mice, RIM cKO^DA 202/4. f, Correlation analyses of transients in d,e (area under the curve, 0 to 600 ms after stimulation), RIM control 203/4, RIM cKO^DA 198/4. g–i, Individual (event heatmaps, top) and average (bottom) time courses of velocity amplitudes (g), and of GCaMP6s (h) and RdLight1 (i) fluorescence during contralateral movement initiations. Event heatmaps in g were sorted by the peak velocity amplitude, and in h,i by the peak amplitude of GCaMP6s in h, RIM control 563/4, RIM cKO^DA 599/4. j–n, Analyses of peaks from d,e, and g–i for each mouse, n as in b,c. There was a strong positive correlation in RIM control mice between GCaMP6s and RdLight1 fluctuations that was disrupted in RIM cKO^DA mice (c). Field illuminations induced dopamine axonal GCaMP6s transients in both genotypes, but failed to trigger dopamine release in RIM cKO^DA mice (d–f). Axonal Ca²⁺ dynamics and striatal dopamine fluctuations correlated during contralateral turns in RIM control mice. In RIM cKO^DA mice, only Ca²⁺ transients, not movement-associated dopamine transients, were detected (g–i). Together with Extended Data Fig. 4, the data suggest that dopamine neuron firing and the underlying regulatory network are not strongly disrupted in RIM cKO^DA mice. Data are mean ± SEM; * p < 0.05, *** p < 0.001, assessed by: two-sided Mann-Whitney rank-sum tests for areas under the curve in c, j–n.