Fig. 4

Synaptic transmission^{Aldh1a1 → EGNIS} mediates delay of gratification. a, The expression of Gi-ChR2 and GFP in Aldh1a1 neurons (Aldh1a1^Gi-ChR2) and EGNIS (EGNIS^GFP), respectively. b, The illustration shows IPSCs were recorded from GFP-expressing EGNIS and evoked by the delivery of blue laser light onto axon terminals of Aldh1a1^Gi-ChR2 neurons. Chemogenetic inhibition of Aldh1a1 axon terminals was achieved by infusing CNO at a concentration of 5 μM. c, Chemogenetic inhibition of synaptic transmission^{Aldh1a1 → EGNIS}. The plot shows the mean amplitude of the evoked IPSCs versus the time of the individual recordings (blue) and the averages (red, mean ± SEM, n = 12 recordings/6 mice) of the evoked IPSCs without (baseline) or with CNO. Three representative traces are the averages of 5 min recordings from the baseline or the presence of CNO. d, Aldh1a1^tdT or Aldh1a1^Gi mice, in which tdT or Gi was expressed in Aldh1a1 neurons were infused of 1 μl of CNO at a concentration of 500 μM or saline into IS 30 mice before behavioral testing, resulting in synaptic terminal silencing. e, Chemogenetic inhibition of Aldh1a1 synaptic outputs reduces the behavioral preference for LDR. The plots show the percentage of the correct trials with the behavioral options for SIR, LDR, or LLR of Aldh1a1^tdT mice with CNO (blue), Aldh1a1^Gi mice with CNO (red), or Aldh1a1^Gi mice with saline (green) at each day of the probe trials (mean ± SEM, n = 9 mice per group). f, The chemogenetic inhibition of Aldh1a1 synaptic projections reduce the percentage of LRA visits. The plot shows the percentage of LRA visits at a delay of 0-3 s (blue) or 6-9 s (red) from the individual (circles) Aldh1a1^tdT mice with CNO or Aldh1a1^Gi- mice with CNO or Aldh1a1^Gi mice with saline and their averages per group (triangles, mean ± SEM, n = 11 mice/group) at day three of the testing sessions. g, EGNIS was expressed with Gi (EGNIS^Gi) in Aldh1a1^−/− mice. h, Chemogenetic inhibition of postsynaptic EGNIS in Aldh1a1^−/− mice increases the behavioral preference for LDR. The plot shows the percentage of the correct trials with the behavioral options for SIR or LDR of Aldh1a1^+/+ mice or Aldh1a1^−/− mice with the expression of Gi in EGNIS (EGNIS^Gi) infused with CNO (blue or green) or saline (red) at each day of the probe trials (mean ± SEM, n = 9 mice per group). i, Chemogenetic inhibition of postsynaptic EGNIS in Aldh1a1^−/− mice increases the percentage of LRA visiting. The plot shows the percentage of LRA visits at a delay of 0-3 s (blue) or 6-9 s (red) from individual (circles) Aldh1a1^+/+ mice or Aldh1a1^−/− mice with the expression of Gi in EGNIS (EGNIS^Gi) infused with CNO or saline and their averages per group (triangles, mean ± SEM, n = 11 mice/group) at day three of the testing sessions. All statistical data are summarized in Supplementary Table 1