Fig. 7: Optogenetic inhibition of SLD orexin signaling shortens REM sleep bouts.

a Schematic drawing of fiber photometry recordings in the SLD orexin terminals. b Representative viral infections of jGCaMP7b (green) in the LH orexin-A+ neurons (blue) (top, scale bar: 25 μm), and optical fiber location above the SLD orexin terminals (bottom, scale bar: 100 μm). c Representative jGCaMP fluorescence traces of the SLD orexin terminals, spectrogram of EEG recordings, and raw EMG recorded simultaneously in a episode of REM sleep (R), the preceding NREM sleep (NR), and the following wakefulness (W). d Averaged changes of jGCaMP fluorescence in REM sleep, the preceding NREM sleep, and the following wakefulness (n = 7 mice; one-way repeated-measures ANOVA; F(2, 12) = 16.758, P = 3.358 × 10−4; post hoc LSD comparison test; REM vs. NREM: P = 2.481 × 10−4; wake vs. NREM: P = 4.563 × 10−3; REM vs. wake: P = 0.0127). e Schematic drawing for optogenetic inhibition of the SLD orexin terminals (left) and procedures for closed-loop optogenetic inhibition during REM sleep (right). The EEG/EMG signals were visually inspected on-line. Lasers were manually turned on with 50% probability after the detection of REM sleep (~10 s), and turned off when the REM sleep episode ended. f Effects of optical inhibition of the SLD orexin terminals during REM sleep on the EEG theta power (left, two-sided paired t-test; t8 = 2.582; P = 0.0325) and EMGREM/NREM ratio (right, two-sided paired t-test; t8 = 1.060; P = 0.320) (n = 9 orexinArchT mice). g Effects of optical inhibition of the SLD orexin terminals during REM sleep on the episode duration of REM sleep (n = 9 orexinArchT mice, two-sided paired t-test; t8 = 2.512; P = 0.0363). Data represent mean ± SEM. *P < 0.05; **P < 0.01. Source data are provided as a Source Data file.