Fig. 7: DVC hyperpolarizes PVP to facilitate backward movement.

a, b Upper: Schematic diagram of the neuron-patch recording setup, showing excitation of DVC and simultaneous recording of the membrane potential in AVB (a) and PVP (b). Lower: Representative membrane potential traces and comparisons of the membrane potential between the illumination and preillumination phases (n = 5 animals in each group). Activation of DVC caused hyperpolarization of PVP but did not affect AVB. Yellow shaded, light stimulation. ***p < 0.001; ns, not significant; two-tailed Student’s t test. Error bars, SEM. c, e Heatmaps showing the proportion of DVC-evoked reversal movements. Optogenetic inhibition of PVP (c) and histamine inhibition of PVP (e) increased the proportion of reversals. Gradually increasing blue light intensity was applied. d, f Plots of the reversal response proportion versus light intensity in (c, e), respectively, showing downward shifts in the activation curves following the inhibition of PVP. The 50% activation intensity in (d) was 3.39 mW/cm² (Control) and 1.31 mW/cm² (PVP::gtACR2). In (f), it was 2.89 mW/cm² without histamine and 1.73 mW/cm² with histamine. n = 10 animals per trial, 8 trials in total, biological replicates in (d, f). Error bars, SEM. g Heatmap showing the proportion of DVC-evoked reversal movements following activation of PVP. h An upward shift in the reversal response proportion curve was observed after light illumination to activate PVP. The 50% activation intensity was 2.89 mW/cm² (Control) and 5.72 mW/cm² (PVP::Chrimson). Nonlinear regression analysis was used to analyze the 50% activation intensity. n = 10 animals per trial, 8 trials in total. Error bars, SEM. i Diagram illustrating the functional neural circuit between DVC and PVP. Inhibiting PVP enhanced DVC-induced backward locomotion, emphasizing the role of PVP in modulating DVC-triggered motor responses. Source data are provided as a Source Data file.