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Bright light exposure suppresses feeding and weight gain via a visual circuit linked to the lateral hypothalamus

Nature Neuroscience volume 29, pages 632–646 (2026) Cite this article

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Abstract

Environmental light regulates nonimage-forming functions like feeding, and bright light therapy shows anti-obesity potential, yet its neural basis remains unclear. Here we show that bright light treatment effectively reduces food intake and mitigates weight gain in mice through a visual circuit involving the lateral hypothalamic area (LHA). Specifically, a subset of SMI-32-expressing ON-type retinal ganglion cells innervate GABAergic neurons in the ventral lateral geniculate nucleus (vLGN), which in turn inhibits GABAergic neurons in the LHA. Activation of both vLGN-projecting retinal ganglion cells and the vLGN-to-LHA projection is sufficient to suppress food consumption and attenuate weight gain. Notably, we provide direct evidence that the suppressive effects of bright light treatment on food consumption and weight gain rely on the activation of the retina–vLGN–LHA pathway. Together, our results delineate an LHA-related visual circuit underlying the food consumption-suppressing and weight gain-attenuating effects of bright light treatment.

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Fig. 1: Bright light treatment suppressed food consumption and attenuated weight gain.
The alternative text for this image may have been generated using AI.
Fig. 2: Activation of the vLGN is essential for the food consumption-suppressing and weight gain-attenuating effects of bright light treatment.
The alternative text for this image may have been generated using AI.
Fig. 3: Activation of the vLGN–LHA pathway is essential for the food consumption-suppressing and weight gain-attenuating effects of bright light treatment.
The alternative text for this image may have been generated using AI.
Fig. 4: vLGN neurons inhibit LHA GABAergic neurons through direct projections.
The alternative text for this image may have been generated using AI.
Fig. 5: Activation of LHA-projecting vLGN neurons reduces food intake.
The alternative text for this image may have been generated using AI.
Fig. 6: Activation of retinal–vLGN–LHA pathway essential for mediating the inhibitory effects of light treatment on feeding behavior.
The alternative text for this image may have been generated using AI.
Fig. 7: Activation of the retina–vLGN–LHA pathway is essential for food consumption-suppressing and weight gain-attenuating effects of bright light treatment.
The alternative text for this image may have been generated using AI.
Fig. 8: Activation of the vLGN–LHA–l/vlPAG pathway is essential for the food consumption-suppressing and weight gain-attenuating effects of bright light treatment.
The alternative text for this image may have been generated using AI.

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Data availability

The data that support the findings of this study are available from the corresponding author upon request. Source data are provided with this paper.

Code availability

The present study did not use any customized code or mathematical methods.

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Acknowledgements

We acknowledge support from the National Natural Science Foundation of China (32171009, 32325022, 31922030, 32171010, 31771170, 82572925, 82172530, 82471263 and 82571736), STI2030-Major Projects (2021ZD0203100), Guangdong Basic and Applied Basic Research Foundation (2021B1515020035, 2023B1515040010, 2023A1515010478 and 2024A1515030204), Science and Technology Program of Guangdong (2018B030334001), Science and Technology Program of Guangzhou (202102070001 and 202007030012), China Postdoctoral Science Foundation (2024M761167), Programme of Introducing Talents of Discipline to Universities (B14036) and K. C. Wong Education Foundation.

Author information

Author notes

  1. These authors contributed equally: Wen Li, Xiaodan Huang, Jijin Wu, Zhengfang Hu.

  2. These authors jointly supervised this work: Song Lin, Qian Tao, Chaoran Ren, Lu Huang.

Authors and Affiliations

  1. State Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Basic Research Center of Excellence for Natural Bioactive Molecules and Discovery of Innovative Drugs, Department of Neurology and Stroke Center, First Affiliated Hospital of Jinan University, Key Laboratory of CNS Regeneration (Ministry of Education), Guangdong Key Laboratory of Non-human Primate Research, GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China

    Wen Li, Xiaodan Huang, Xiaohuai Xu, Qingguo Lv, Jijin Wu, Zhengfang Hu, Ran Li, Yan Yang, Lijie Yu, Bingjie Liu, Kwok-Fai So, Chaoran Ren & Lu Huang

  2. Experimental Teaching Center of Basic Medicine, School of Basic Medicine and Public Health, Jinan University, Guangzhou, China

    Li Song

  3. Neuroscience and Neurorehabilitation Institute, University of Health and Rehabilitation Sciences, Qingdao, China

    Yue Xi, Kwok-Fai So & Chaoran Ren

  4. Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China

    Kwok-Fai So & Chaoran Ren

  5. Physiology Department, School of Medicine, Jinan University, Guangzhou, China

    Song Lin

  6. Department of Rehabilitation Medicine, First Affiliated Hospital of Jinan University, School of Medicine, Jinan University, Guangzhou, China

    Qian Tao

  7. Emergency Department, Zhujiang Hospital, Southern Medical University, Guangzhou, China

    Lu Huang

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  1. Wen Li
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Contributions

L.H., C.R., Q.T. and S.L. designed the experiments. L.H. and C.R. wrote the manuscript. W.L., X.X., Q.L. and J.W. performed the behavioral experiments. W.L., J.W. and Y.Y. performed the surgery. X.H., J.W. and Z.H. performed physiological recordings. R.L., L.Y., Y.X., S.L., X.X., B.L., Q.L. and J.W. performed histology and microscopy. W.L., L.S., J.W., Q.T., R.L., Q.L., Z.H. and K.-F.S. analyzed the data.

Corresponding authors

Correspondence to Song Lin, Qian Tao, Chaoran Ren or Lu Huang.

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Extended data

Extended Data Fig. 1 Bright light treatment suppresses food consumption and attenuates weight gain without affecting metabolism in mice. Related to Fig. 1.

a, Experimental design for metabolic test under bright light (BL, 3,000 lux, 12-h) exposure. b, Left, time course of cumulative food consumption at room light (RL, 200 lux) and BL exposure was recorded for 24-h; n = 8 mice. Each symbol represents the mean of eight individual mice. Right, quantitative date of cumulative food consumption (n = 8 mice; Light, RL versus BL P = 0.0027; Dark, RL vs. BL P = 0.6967). c-h, Left, energy expenditure (c, EE), respiratory exchange ratio (d, RER), ambulatory movement (e, XAMB), total activity (f, XTOT), oxygen consumed (g, VO2) and carbon dioxide consumed (h, VCO2) of chow-fed mice at RL and BL exposure was recorded for 24-h; n = 8 mice. Right, quantitative date of EE (c; Light, RL vs. BL P = 0.9893; Dark, RL vs. BL P = 0.9769), RER (d; Light, RL vs. BL P = 0.9923; Dark, RL vs. BL P = 0.9077), XAMB (e; Light, RL vs. BL P = 0.9969; Dark, RL vs. BL P = 0.6523), XTOT (f; Light, RL vs. BL P = 0.8885; Dark, RL vs. BL P = 0.1594), VO2 (g; Light, RL vs. BL P = 0.9692; Dark, RL vs. BL P = 0.7253) and VCO2 (h; Light, RL vs. BL P = 0.9953; Dark, RL vs. BL P = 0.9980) is presented as mean ± s.e.m (n = 8 mice). i, Schematic of experimental design for OFT or EPM after 5 days BL (3,000 lux, 12-h) exposure. j, Quantitative of anxiety-like behaviors (n = 8 mice; Center time, RL vs. BL P = 0.1403; Total distance, RL vs. BL P = 0.2567; Open arms duration, RL vs. BL P = 0.7273). k, Left, schematic of experimental design for corticosterone (CORT) test under bright light exposure. Right, time course of serum CORT level (n = 8 mice, RL vs. BL P = 0.4926). l, Changes in serum CORT levels in mice exposure to different durations (left) or light intensities (right) of light treatment (LT) (n = 8 mice; Bright light exposure, 1 h vs. 7 h P = 0.9827, 1 h vs. 12 h P = 0.8893; Light exposure, RL vs. 1,000 lux P = 0.9846, RL vs. 3,000 lux P = 0.8401, RL vs. 5,000 lux P = 0.9693). Two-way ANOVA with Sidak’s multiple-comparisons test was used in b-h (right) and k (right). One-way ANOVA with Sidak’s multiple-comparisons test was used in l. Two-tailed unpaired t-test was used in j. ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

Source data

Extended Data Fig. 2 Bright light treatment suppressed food consumption across both female and male mice. Related to Fig. 1.

a, Schematic of the experimental design in female and male mice. b, 1-h food intake test, food intake assessed following 23-h food-restriction (FR) in female mice exposed to different intensities of light treatment (LT, 0~5,000 lux) (n = 11 mice, 0 lux vs. 200 lux P > 0.9999, 200 lux vs. 1,000 lux P = 0.2456, 200 lux vs. 3,000 lux P = 0.0003, 200 lux vs. 5,000 lux P = 0.0034). c, 1-h (left) or 6-h (right) food intake in FR female and male mice exposed to room light (RL, 200 lux) or bright light (BL, 3,000 lux) (n = 8 mice; 1 h food intake, Female-RL vs. Female-BL P < 0.0001, Female-RL vs. Male-RL P = 0.4845, Male-RL vs. Male-BL P = 0.0003; 6 h food intake, Female-RL vs. Female-BL P = 0.0006, Female-RL vs. Male-RL P = 0.9878, Male-RL vs. Male-BL P = 0.0137). d, Food intake assessed in chow-fed female mice exposure to different intensities of LT (n = 8 mice, 0 lux vs. 200 lux P > 0.9999, 200 lux vs. 1000 lux P = 0.7929, 200 lux vs. 3,000 lux P = 0.0201, 200 lux vs. 5,000 lux P = 0.0246). e-g, Changes in food intake during the daytime (e) and the nighttime (f, RL vs. BL P = 0.8787) of chow-fed female mice under exposure to RL or BL, comparison of percentage body weight change after RL or BL exposure 5 days (g, RL vs. BL P = 0.0021); n = 8 mice. h, k, Schematic of the experimental design for EEG or EMG recording during 2-h bright light exposure (h) or following 5 days of bright light exposure (k). i, Representative EEG and EMG spectrograms of mice in RL and BL groups. j, The quantitation analysis on the time of NREM, WAKE and REM (n = 6 mice; NREM, RL vs. BL P = 0.9977; WAKE, RL vs. BL P = 0.9986, REM, RL vs. BL P > 0.9999). l-o, Time course changes of Wakefulness (l, left), NREM (m, left) and REN (n, left), total wake (l, middle; RL vs. BL P = 0.5339), NREM (m, middle; RL vs. BL P = 0.7725) and REM (n, middle; RL vs. BL P = 0.6637) amounts during the whole day (24-h), total wake (l, right; Light, RL vs. BL P = 0.9989; Dark, RL vs. BL P = 0.8492), NERM (m, right; RL vs. BL P = 0.9381; Dark, RL vs. BL P = 0.9998) and REM (n, right; RL vs. BL P = 0.9387; Dark, RL vs. BL P = 0.9959) amounts during light phase (7 AM-7 PM) and dark phase (7 PM-7 AM), number of transitions between different pair of brain states during the whole day (24-h, o; NREM, RL vs. BL P > 0.9999; WAKE, RL vs. BL P > 0.9999, REM, RL vs. BL P > 0.9999) of mice in RL and BL groups; n = 6 mice. One-way ANOVA with Sidak’s multiple-comparisons test was used in b, c, and d. Two-way ANOVA with Sidak’s multiple-comparisons test was used in e, and f, j, l (right), m (right), n (right) and o. Two-tailed unpaired t-test was used in g, l (middle), m (middle), and n (middle). *P < 0.05; **P < 0.001; ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 3 Optogenetic inhibition of vLGN neurons, the vLGN-LHb pathway, or the vLGN-l/vlPAG pathway is effective in vivo. Related to Fig. 3.

a, Schematic showing hSyn-NpHR-mCherry injected into the vLGN in C57BL/6 mice and in vitro electrophysiology recording. b, 1 sec activation (589 nm, 25 Hz, 5 ms) of NpHR expressed in vLGN neurons inhibits the firing in vitro, but does not induce rebound, the data was repeated three times. c, i, Viral injection and optrode placement for selective inhibition of vLGN-LHb (c) and vLGN-l/vlPAG (i) input during individual trials of feeding behaviors. d, Behavioral paradigm during in vivo optrode recordings. e-g, Rasters and PSTH (bin = 5 ms) of example LHb neuron responses to the air blow with (g) or without (e, f) optogenetic inhibition (15 mW, 25 Hz) of vLGN input to the LHb during room light (e) or bright light (f, g) exposure. h, n, Left, average Z-score trace of LHb neurons (h, n = 48 cells, 4 mice) and l/vlPAG neurons (n, n = 48 cells, 4 mice) that were excited in response to the air blow with (orange) and without (black and rose red) optogenetic inhibition. Neurons excited by the air blow showed a significantly reduced Z-score response during bright light exposure (3,000 lux, constant). Right, column chart shows average peak Z-score of LHb neurons (h; RL-OFF vs. BL-OFF P < 0.0001, BL-OFF vs. BL-ON P = 0.0004) and l/vlPAG (n; RL-OFF vs. BL-OFF P = 0.0005, BL-OFF vs. BL-ON P = 0.0188) neurons for the first 5 s before and after the air blow. j, Behavioral paradigm during in vivo optrode recordings. k–m, Rasters and PSTH (bin = 5 ms) of example l/vlPAG neuron responses to the air blow with (m) or without (k, l) optogenetic inhibition (15 mW, 25 Hz) of vLGN input to the l/vlPAG during room light (k) or bright light (l, m) exposure. One-way ANOVA with Sidak’s multiple-comparisons test was used in all figure. *P < 0.05, ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 4 Activation or suppression of the vLGN-LHA pathway did not induce place preference in real-time place preference tests. Related to Fig. 3.

a, d, Scheme illustration of bilateral optical fiber implantation in the LHA of mice following AAV2/9-hSyn-NpHR-mCherry (a) and AAV2/9-hSyn-ChR2-mCherry (d) injection into the vLGN. b, c, Heatmaps encoding the spatial location of food-restricted (FR) mice with yellow light delivery (15 mW, 25 Hz) during bright light exposure (b), percentage of time spent on the stimulation side during each 10 min (c) (n = 8 mice, OFF vs. ON P = 0.7699, OFF vs. OFF P = 0.7699, ON vs. OFF P = 0.8989). e, f, Heatmaps encoding the spatial location of food-restricted (FR) mice with blue light delivery (15 mW, 20 Hz) during bright light exposure (e), percentage of time spent on the stimulation side (f) during each 5 min (n = 8 mice, OFF vs. ON P = 0.5856, OFF vs. OFF P = 0.8001, ON vs. OFF P = 0.5706). g, j, Scheme illustration of bilateral optical fiber implantation into the LHA of mice following LHA postsynaptic neurons using AAV2/9-Fas-DO-ChR2-eGFP (g) or AAV2/9-DIO-ChR2-eGFP (j); scale bar, 200μm. h, i, Heatmaps of RTPP-associated spatial locations from a fed-chow mouse (h), percentage of time spent on the stimulation side during each 10 min (i, OFF vs. ON P < 0.0001, OFF vs. OFF P = 0.2217, ON vs. OFF P < 0.0001); n = 8 mice. k, l, RTPP Heatmaps encoding the spatial location from a chow-fed mouse (k), percentage of time spent on the stimulation side during each 10 min (l, OFF vs. ON P = 0.6991, OFF vs. OFF P = 0.1332, ON vs. OFF P = 0.1815); n = 8 mice. m. Schematic of the experimental design for suppressing vLGN-LHb or vLGN-l/vlPAG pathway during 1-h or 6-h acute feeding test. n, Scheme specific for l/vlPAG-projecting vLGN with hM4Di; scale bar, 200 μm. o, Food intake assessment during 1-h (left, hM4Di-RL-SAL vs. hM4Di-BL-SAL, P = 0.0010, hM4Di-BL-SAL vs. hM4Di-BL-CNO, P = 0.9857) and 6-h (right, hM4Di-RL-SAL vs. hM4Di-BL-SAL, P = 0.0021, hM4Di-BL-SAL vs. hM4Di-BL-CNO, P = 0.5598) feeding test; n = 8 mice. p, Scheme for specific targeting LHb-projecting vLGN with hM4Di. q, Food intake assessment during 1-h (left, hM4Di-RL-SAL vs. hM4Di-BL-SAL, P = 0.0015, hM4Di-BL-SAL vs. hM4Di-BL-CNO, P = 0.3321) and 6-h (right, hM4Di-RL-SAL vs. hM4Di-BL-SAL, P = 0.0001, hM4Di-BL-SAL vs. hM4Di-BL-CNO, P = 0.7513) feeding test; n = 8 mice. One-way ANOVA with Sidak’s multiple-comparisons test was used in all figure. ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 5 vLGN neurons inhibit LHA GABAergic neurons through direct projections. Related to Fig. 4.

a, Left, scheme for specific labeling of LHA-projecting vLGN neurons with eGFP. Right, representative images of the vLGN and LHA 2 weeks after virus injections, in which the location of the injection site of rAAV2/2-Retro-Cre was visualized with CTB-647. Scale bar, 200 μm. b, A representative example of LHA-projecting vLGN neurons labeled with eGFP (number indicate distance from bregma). Scale bar, 200 μm. c, Left, representative images of the vLGN illustrating eGFP-expressing vLGN neurons co-labeled with GABAergic neurons. Right, pie chart indicates percentage of eGFP-expressing vLGN neurons co-labeled with GABAergic neurons; n = 5 mice. Scale bar, 50 μm. d, Left, scheme for specific labeling of LHA neurons receiving direct vLGN inputs with eGFP. Right, representative images of injection site of vLGN and LHA. Scale bar, 200 μm. e, Representative example showing LHA postsynaptic neurons with eGFP. Scale bar, 200 μm. f, Left, a representative images of LHA illustrating eGFP-expressing LHA neurons co-labeled with GABAergic neurons. Right, pie chart indicates percentage of eGFP-expressing LHA neurons co-labeled with GABAergic neurons; n = 5 mice. Scale bar, 50 μm. g, Scheme showing specific unilateral infection of vLGN GABAergic neurons with eGFP using vGAT-Cre mice. Scale bar, 200 µm. h, Representative images showing the downstream areas projection by vLGN GABAergic neurons. Scale bar, 200 µm. i, Labeling of vLGN GABAergic neurons with DIO-ChR2 and LHA GABAergic neurons with DIO-eGFP in vGAT-Cre mice. j, Representative images of LHA GABAergic neurons and fiber connections from vLGN GABAergic neurons. Scale bar, 200 μm (Left) and 50 μm (Right). k, Optogenetically evoked IPSCs in LHA GABAergic neurons expressing eGFP; n = 38 cells from four mice.

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Extended Data Fig. 6 Activation of the vLGN GABAergic is essential for the food consumption-suppressing and weight gain-attenuating effects of bright light treatment. Related to Fig. 4.

a, Scheme for specific infection of vLGN GABAergic neurons with hM4Di or mCherry. Scale bar, 200 μm. b, Current-evoked action potentials in a representative hM4Di-infected vLGN GABAergic neurons recorded before, during, and after CNO perfusion (10 μM) (n = 5 cells from two mice, ACSF vs. CNO P = 0.0015, CNO vs, Washout P = 0.0035). c-e, Changes in food intake during daytime (c) and nighttime (d) in different groups of chow-fed mice, and body weight changes in 5 consecutive weeks (e, 2 weeks P = 0.9998, 3 weeks P = 0.2854, 4 weeks P = 0.0466, 5 weeks P = 0.1568), i.p. CNO injections during fifth week (e); n = 8 mice. f, g, 1-h (f, hM4Di-RL-Saline vs. hM4Di-BL-Saline P = 0.0064, hM4Di-BL-Saline vs. hM4Di-BL-CNO P = 0.0026) and 6-h feeding test (g, hM4Di-RL-Saline vs. hM4Di-BL-Saline P = 0.0020, hM4Di-BL-Saline vs. hM4Di-BL-CNO P = 0.0020) in different groups; n = 8 mice. h, Scheme for specific infection of vLGN GABAergic neurons with hM3Dq or eGFP. Scale bar, 200 μm. i, vLGN neurons expressing hM3Dq can be activated by bath application of CNO (10 μM) (n = 5 cells from two mice, ACSF vs. CNO P = 0.0017). j, Schematic of experimental design of the chow-fed model. k–m, Changes in food intake during daytime (k) and nighttime (l, mCherry vs. hM3Dq P = 0.9865) of chow-fed mice; n = 8 mice, body weight change following 5 consecutive days of CNO i.p. injections (m, mCherry-CNO vs. hM3Dq-CNO P = 0.0010); n = 8 mice. n. Schematic of experimental design of the food-restriction model. o, p, 1-h (o, mCherry-CNO vs. hM3Dq-CNO P = 0.0007) and 6-h feeding test (p, mCherry-CNO vs. hM3Dq-CNO P = 0.0046) in different groups; n = 8 mice. q, Schematic of the experimental design for optogenetically suppressing the vLGN-LHA pathway during 1-h or 6-h acute feeding tests in vGAT-Cre mice. r, Schematic representation of the viral strategy used to inhibit the vLGN-LHA GABAergic neurons projections. s, Optogenetic inhibition (15 mW, 25 Hz) of vLGN-LHA GABAergic projections during BL exposure (3,000 lux) in FR mice (n = 9 mice; Food intake, OFF vs. ON P = 0.0004, ON vs. OFF P = 0.0011; Latency, OFF vs. ON P = 0.0158, ON vs. OFF P = 0.0136; Total time spent feeding OFF vs. ON P = 0.0004, ON vs. OFF P = 0.0031). One-way ANOVA with Sidak’s multiple-comparisons test was used in b (right), f, g, and s. Two-way ANOVA with Sidak’s multiple-comparisons test was used in c, d, e, k, and l. Two-tailed unpaired t-test was used in m, o, and p. Two-tailed paired t-test was used in i (right). *P < 0.05; **P < 0.001; ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 7 Bright light treatment inhibits the excitatory effect of food intake on LHA neurons. Related to Fig. 6.

a, Illustration of unilateral implantation of an optical fiber in the LHA of mice receiving vLGN inhibition with hM4Di. Scale bar, 200 μm. b, Schematic representation of the experimental timeline designed for recording feeding behavior using fiber photometry under BL exposure (3,000 lux). c, Experimental model for recording feeding behavior using fiber photometry under BL exposure (3,000 lux). d, Average photometry trace for mice approaching food in different groups; n = 9 mice. e, Left, heatmap showing photometry recordings from different trials of mice approaching food; n = 9 mice. Right, the peak amplitude of the Ca2+ signal (n = 9 mice, RL-Saline vs. BL-Saline P = 0.0092, BL-Saline vs. BL-CNO, P = 0.0022). f, Illustration of recording calcium activity in the LHA following retinal inhibition and representative images of location of virus injection. Scale bar, 200 μm. g, Left, representative images of specific labeling of vLGN-projecting RGCs with hM4Di-mCherry. Right, i.p. injection of CNO (1 mg/kg) decreased BL-induced c-Fos expression in vLGN-projecting RGCs (n = 8 sections from four mice, Saline vs. CNO P < 0.0001). Scale bar, 200 μm (Left) and 25 μm (Left). h, Experimental model for recording feeding behavior using fiber photometry under BL exposure (3,000 lux). i, Average photometry trace for mice approaching food in different groups; n = 8 mice. j, Left, heatmap showing photometry recordings different trials of mice approaching food and peak amplitude of Ca2+ signal (n = 8 mice, RL-Saline vs. BL-Saline P = 0.0015, BL-Saline vs. BL-CNO, P = 0.0018). One-way ANOVA with Sidak’s multiple-comparisons test was used in e (right) and j (right). Two-tailed unpaired t-test was used in g (right). **P < 0.001; ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 8 Divergent regulation of l/vlPAG by two distinct vLGN-derived circuits: vLGN-l/vlPAG and vLGN-LHA-l/vlPAG pathways engage non-overlapping cellular populations. Related to Fig. 8.

a, Left, rabies virus tracing the l/vlPAG receiving input from the LHA. Right, injection site of l/vlPAG illustrating the star cells (yellow). Scale bar, 200 μm (upper), 50 μm (bottom). b, Representative images of the areas projecting to the l/vlPAG that receive input from the LHA. Scale bar, 200 μm. Right, quantifications of neurons projecting to the l/vlPAG in different brain regions (n = 4 mice). c, Specific injection of l/vlPAG postsynaptic neurons with DIO-hM3Dq or DIO-eGFP. Scale bar, 200 μm. d-f, Changes in food intake during the daytime (d) and the nighttime (e, eGFP vs. hM3Dq P = 0.6079) in chow-fed mice; n = 8 mice. Weekly time course of body weight (f, 2 weeks P = 0.6414, 3 weeks P < 0.0001); n = 8 mice. g, h, 1-h (g, P < 0.0001) and 6-h (h, P = 0.0217) food intake test in chow-fed mice; n = 8 mice. i-l, Depressive- and anxiety-like behaviors in different experimental groups; n = 7 mice. OFT (i; Center time, P = 0.5367, Total time, P = 0.2673), EPM (j, P = 0.4570), forced swim test (FST) (k, P = 0.6917), and tail suspension test (TST) (l, P = 0.9249). m, Mice were injected with l/vlPAG postsynaptic neurons using DO-hM3Dq or DO-eGFP, which do not target neurons receiving direct inputs from the LHA. Scale bar, 200 μm. n, o, OFT (n; Center time, P < 0.0001, Total time, P = 0.0001), EPM (o, P < 0.0001) in different experimental groups; n = 7 mice. Two-way ANOVA with Sidak’s multiple-comparisons test was used in d, e, and f. Two-tailed unpaired t-test was used in g-o. *P < 0.05; **P < 0.001; ***P < 0.0001; ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Extended Data Fig. 9 Activation of the vLGN-LHA-l/vlPAG pathway did not induce place preference in real-time place preference tests. Related to Fig. 8.

a, Schematic illustration of bilateral optical fiber implantation in the l/vlPAG of mice following injection of AAV2/9-DIO-ChR2-mCherry into the LHA receiving input from the vLGN. b, Upper, schematic representation of the RTPP paradigm without food intake, food-restriction (FR) mice were conditioned to associate stimulation side of the chamber with blue light delivered (15 mW, 20 Hz) during BL exposure. Bottom, heatmaps encoding spatial location from a FR mouse during free exploration on each side. c, Percentage of time spent on the stimulation side during pre-optogenetic stimuli, optogenetic stimuli and post-optogenetic stimuli phases, with each phase lasting 10 min continuously (n = 8 mice, OFF vs. ON P = 0.8900, OFF vs. OFF P = 0.8900, OFF vs. ON P = 0.8900). One-way ANOVA with Sidak’s multiple-comparisons test was used in all figure. ns, no significant difference. All error bars indicate the mean ± s.e.m. Detailed statistical information is available in Supplementary Table 1.

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Unprocessed source data of feeding behaviors, food intake, body weight and anxiety-like behavior.

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Unprocessed source data of optical fiber recording, electrophysiology in vitro, food intake and body weight.

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Unprocessed source data of electrophysiology in vitro and optical fiber recording.

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Unprocessed source data of electrophysiology in vitro, food intake and body weight.

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Li, W., Huang, X., Xu, X. et al. Bright light exposure suppresses feeding and weight gain via a visual circuit linked to the lateral hypothalamus. Nat Neurosci 29, 632–646 (2026). https://doi.org/10.1038/s41593-025-02156-1

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