[{"OA_type":"closed access","external_id":{"pmid":["41494523"]},"article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"AmDo"},{"_id":"SiHi"}],"day":"05","publication_identifier":{"eissn":["1879-0445"],"issn":["0960-9822"]},"status":"public","scopus_import":"1","pmid":1,"publication":"Current Biology","year":"2026","volume":36,"doi":"10.1016/j.cub.2025.11.056","intvolume":"        36","author":[{"first_name":"Hakan","full_name":"Kücükdereli, Hakan","id":"5d5f6ea4-ef9e-11f0-a10a-85e12a3552af","last_name":"Kücükdereli"},{"orcid":"0000-0001-5398-6473","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","last_name":"Douglass","full_name":"Douglass, Amelia May Barnett","first_name":"Amelia May Barnett"}],"date_created":"2026-01-11T23:01:33Z","title":"Neuroscience: What doesn’t kill you makes you stronger","issue":"1","date_published":"2026-01-05T00:00:00Z","article_type":"letter_note","date_updated":"2026-01-12T10:09:13Z","language":[{"iso":"eng"}],"publisher":"Elsevier","quality_controlled":"1","oa_version":"None","corr_author":"1","page":"R27-R29","citation":{"short":"H. Kücükdereli, A.M. Douglass, Current Biology 36 (2026) R27–R29.","apa":"Kücükdereli, H., &#38; Douglass, A. M. (2026). Neuroscience: What doesn’t kill you makes you stronger. <i>Current Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cub.2025.11.056\">https://doi.org/10.1016/j.cub.2025.11.056</a>","chicago":"Kücükdereli, Hakan, and Amelia M. Douglass. “Neuroscience: What Doesn’t Kill You Makes You Stronger.” <i>Current Biology</i>. Elsevier, 2026. <a href=\"https://doi.org/10.1016/j.cub.2025.11.056\">https://doi.org/10.1016/j.cub.2025.11.056</a>.","ista":"Kücükdereli H, Douglass AM. 2026. Neuroscience: What doesn’t kill you makes you stronger. Current Biology. 36(1), R27–R29.","ama":"Kücükdereli H, Douglass AM. Neuroscience: What doesn’t kill you makes you stronger. <i>Current Biology</i>. 2026;36(1):R27-R29. doi:<a href=\"https://doi.org/10.1016/j.cub.2025.11.056\">10.1016/j.cub.2025.11.056</a>","mla":"Kücükdereli, Hakan, and Amelia M. Douglass. “Neuroscience: What Doesn’t Kill You Makes You Stronger.” <i>Current Biology</i>, vol. 36, no. 1, Elsevier, 2026, pp. R27–29, doi:<a href=\"https://doi.org/10.1016/j.cub.2025.11.056\">10.1016/j.cub.2025.11.056</a>.","ieee":"H. Kücükdereli and A. M. Douglass, “Neuroscience: What doesn’t kill you makes you stronger,” <i>Current Biology</i>, vol. 36, no. 1. Elsevier, pp. R27–R29, 2026."},"type":"journal_article","month":"01","_id":"20972","abstract":[{"text":"Small amounts of stress are thought to have beneficial effects. A new study reports a mechanism by which the psychedelic drug, psilocybin, causes acute release of stress hormones, despite its known long-term anti-anxiety effects.","lang":"eng"}]},{"OA_place":"publisher","DOAJ_listed":"1","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","_id":"21744","abstract":[{"text":"The paraventricular hypothalamus (PVH) controls behavioral and physiologic processes, including appetite, social behavior, autonomic outflow, and pituitary hormone secretion. However, molecular markers for centrally projecting PVH neuron populations remain largely undefined, and a complete census of PVH cell types has not been established. Therefore, we performed extensive single-cell/nucleus RNA sequencing to catalog PVH neuron subtypes and multiplexed error-robust fluorescence in situ hybridization (MERFISH) to map them spatially. Our spatial transcriptomic atlas resolves 26 Sim1+ and 29 GABAergic neuron populations from the PVH and surrounding areas. Additionally, projection-based profiling identified neurons that project to the parabrachial region (PB) and spinal cord, helping to determine PVH populations that regulate satiety and sympathetic nervous system activity, respectively. Notably, activation of PB-projecting PVH neurons expressing Brs3 reduces food intake, and silencing them causes obesity. Together, this atlas contributes high-resolution PVH spatial and circuit-based gene expression profiles, representing a valuable resource for the field of homeostasis.","lang":"eng"}],"oa":1,"month":"02","type":"journal_article","citation":{"short":"Y. Li, T.C. Butler, S. Nardone, C.L. Jacobs, A.M. Douglass, J.C. Madara, M.C. McDonough, J. Tao, E.D. Lowenstein, L. Wang, D. Pant, S.J. Walker, A. Wang, H. Srinivasan, Z. Yang, J.N. Campbell, L.T. Tsai, B.B. Lowell, J.M. Resch, Cell Reports 45 (2026).","apa":"Li, Y., Butler, T. C., Nardone, S., Jacobs, C. L., Douglass, A. M., Madara, J. C., … Resch, J. M. (2026). A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2025.116904\">https://doi.org/10.1016/j.celrep.2025.116904</a>","ama":"Li Y, Butler TC, Nardone S, et al. A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types. <i>Cell Reports</i>. 2026;45(2). doi:<a href=\"https://doi.org/10.1016/j.celrep.2025.116904\">10.1016/j.celrep.2025.116904</a>","chicago":"Li, Yuxi, Trevor C. Butler, Stefano Nardone, Christopher L. Jacobs, Amelia M. Douglass, Joseph C. Madara, Miriam C. McDonough, et al. “A Spatial and Projection-Based Transcriptomic Atlas of Paraventricular Hypothalamic Cell Types.” <i>Cell Reports</i>. Elsevier, 2026. <a href=\"https://doi.org/10.1016/j.celrep.2025.116904\">https://doi.org/10.1016/j.celrep.2025.116904</a>.","ista":"Li Y, Butler TC, Nardone S, Jacobs CL, Douglass AM, Madara JC, McDonough MC, Tao J, Lowenstein ED, Wang L, Pant D, Walker SJ, Wang A, Srinivasan H, Yang Z, Campbell JN, Tsai LT, Lowell BB, Resch JM. 2026. A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types. Cell Reports. 45(2), 116904.","mla":"Li, Yuxi, et al. “A Spatial and Projection-Based Transcriptomic Atlas of Paraventricular Hypothalamic Cell Types.” <i>Cell Reports</i>, vol. 45, no. 2, 116904, Elsevier, 2026, doi:<a href=\"https://doi.org/10.1016/j.celrep.2025.116904\">10.1016/j.celrep.2025.116904</a>.","ieee":"Y. Li <i>et al.</i>, “A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types,” <i>Cell Reports</i>, vol. 45, no. 2. Elsevier, 2026."},"publisher":"Elsevier","quality_controlled":"1","oa_version":"Published Version","tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"date_updated":"2026-05-04T12:00:31Z","language":[{"iso":"eng"}],"acknowledgement":"We would like to thank Drs. Mark Andermann, Joel Geerling, and Clifford\r\nSaper, as well as the Lowell, Tsai, and Resch laboratories for helpful discussions;\r\nAlysia Berns, Jia Yu, and Yanfang Li for technical support; the BNORC\r\nFunctional Genomics and Bioinformatics Core (P30DK046200) and the Iowa\r\nInstitute for Human Genetics Genomics Division (IIHG, RRID: SCR_023422)\r\nfor helpful discussions and technical assistance with sc/snRNA-seq; Zachary\r\nNiziolek and the Bauer Core Facility at Harvard University, the BIDMC Flow Cytometry\r\nCore, and Heath Vignes, Michael Shey, and Thomas Kaufman of the\r\nFlow Cytometry Facility at the University of Iowa Carver College of Medicine\r\nfor helpful discussions and technical support; the ICCB-Longwood Screening\r\nFacility of Harvard Medical School for assistance with the snRNA-seq\r\nexperiments; Dr. Sayak Mitter and Vizgen support for technical assistance\r\nwith the MERSCOPE platform; and Mara Jendro and Li-Chun (Queena) Lin\r\nfor their assistance with MERSCOPE experiments within the Iowa\r\nNeuroBank Core in the Iowa Neuroscience Institute at the University of Iowa\r\nCarver College of Medicine. This research was funded by the following NIH\r\ngrants to L.T.T.: R01DK128406; to B.B.L.: R01DK075632, R01DK134427,\r\nand R01DK096010; to J.M.R.: R00HL144923 and R01NS141072; and to M.C.M.: F31HL170784; T.C.B. and M.C.M. were supported by a pharmacological\r\nsciences predoctoral training grant T32GM144636. Additional funding\r\nto J.M.R. came from the American Heart Association (AHA 935362), a University\r\nof Iowa Fraternal Order of Eagles Diabetes Research Center Pilot and\r\nFeasibility Catalyst Grant, and an Iowa Neuroscience Institute Early Stage\r\nInvestigator award from the Carver Trust. Y.L. was supported by a predoctoral\r\nfellowship from the American Heart Association (AHA 25PRE1372983). A.M.D.\r\nwas supported by a postdoctoral fellowship from the Charles A. King Trust.","doi":"10.1016/j.celrep.2025.116904","ddc":["570"],"intvolume":"        45","scopus_import":"1","pmid":1,"year":"2026","publication":"Cell Reports","volume":45,"date_published":"2026-02-24T00:00:00Z","article_type":"original","date_created":"2026-04-16T13:51:29Z","article_number":"116904","title":"A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic cell types","author":[{"last_name":"Li","first_name":"Yuxi","full_name":"Li, Yuxi"},{"last_name":"Butler","full_name":"Butler, Trevor C.","first_name":"Trevor C."},{"last_name":"Nardone","full_name":"Nardone, Stefano","first_name":"Stefano"},{"full_name":"Jacobs, Christopher L.","first_name":"Christopher L.","last_name":"Jacobs"},{"first_name":"Amelia May Barnett","full_name":"Douglass, Amelia May Barnett","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","last_name":"Douglass","orcid":"0000-0001-5398-6473"},{"last_name":"Madara","first_name":"Joseph C.","full_name":"Madara, Joseph C."},{"full_name":"McDonough, Miriam C.","first_name":"Miriam C.","last_name":"McDonough"},{"first_name":"Jenkang","full_name":"Tao, Jenkang","last_name":"Tao"},{"last_name":"Lowenstein","full_name":"Lowenstein, Elijah D.","first_name":"Elijah D."},{"last_name":"Wang","first_name":"Luhong","full_name":"Wang, Luhong"},{"full_name":"Pant, Deepti","first_name":"Deepti","last_name":"Pant"},{"last_name":"Walker","first_name":"Samuel J.","full_name":"Walker, Samuel J."},{"last_name":"Wang","first_name":"Annette","full_name":"Wang, Annette"},{"last_name":"Srinivasan","first_name":"Harini","full_name":"Srinivasan, Harini"},{"last_name":"Yang","first_name":"Zongfang","full_name":"Yang, Zongfang"},{"full_name":"Campbell, John N.","first_name":"John N.","last_name":"Campbell"},{"full_name":"Tsai, Linus T.","first_name":"Linus T.","last_name":"Tsai"},{"last_name":"Lowell","full_name":"Lowell, Bradford B.","first_name":"Bradford B."},{"full_name":"Resch, Jon M.","first_name":"Jon M.","last_name":"Resch"}],"issue":"2","file":[{"file_id":"21793","access_level":"open_access","success":1,"content_type":"application/pdf","checksum":"82098dd9d0ca609119f9f2c6beb4fc1e","relation":"main_file","date_updated":"2026-05-04T11:58:51Z","file_name":"2026_CellReports_Li.pdf","date_created":"2026-05-04T11:58:51Z","creator":"dernst","file_size":38532865}],"OA_type":"gold","file_date_updated":"2026-05-04T11:58:51Z","publication_identifier":{"issn":["2639-1856"],"eissn":["2211-1247"]},"day":"24","status":"public","has_accepted_license":"1","publication_status":"published","external_id":{"pmid":["41581146"]},"department":[{"_id":"AmDo"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes"},{"year":"2026","publication":"Neuron","scopus_import":"1","pmid":1,"acknowledgement":"We thank all members of the B.B.L. laboratory for helpful discussions. We\r\nthank the BADERC and BNORC transgenic cores (NIH P30DK057521 and\r\nP30DK046200) for performing embryo injections to generate knockin mouse\r\nlines. We also thank the BIDMC Energy Balance Core (supported by NIH\r\nS10OD028635 and the Boston Area Diabetes Endocrinology Research Centers, P30DK135043), where Marissa Cortopassi performed indirect calorimetry experiments and Alexander Banks assisted with data analysis and interpretation. Confocal imaging was performed at BIDMC’s Confocal Imaging\r\nCore. We thank Chen Wu for assistance in designing knockin mouse lines.\r\nThis work was supported by the NIH (R01DK134427, R01DK096010, and\r\nR01DK075632 to B.B.L.). Authors were supported by an EMBO Long-Term\r\nFellowship (770-2018, S.J.W.), a T32 Postdoctoral Training Fellowship\r\n(5T32DK007516, E.D.L.), the Charles A. King Trust Postdoctoral Research\r\nFellowship program (A.M.D.), and a K99 Career Development Award\r\n(K99HL144923, J.M.R.).","doi":"10.1016/j.neuron.2026.05.010","title":"A hypothalamic circuit for anticipating future changes in energy balance","author":[{"last_name":"Walker","first_name":"Samuel J.","full_name":"Walker, Samuel J."},{"full_name":"Lowenstein, Elijah D.","first_name":"Elijah D.","last_name":"Lowenstein"},{"full_name":"Douglass, Amelia May Barnett","first_name":"Amelia May Barnett","orcid":"0000-0001-5398-6473","last_name":"Douglass","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289"},{"last_name":"Thomas","first_name":"Callum M.P.","full_name":"Thomas, Callum M.P."},{"last_name":"Madara","first_name":"Joseph C.","full_name":"Madara, Joseph C."},{"last_name":"Kucukdereli","first_name":"Hakan","full_name":"Kucukdereli, Hakan"},{"last_name":"Barbosa-Meillon","first_name":"Eunice A.","full_name":"Barbosa-Meillon, Eunice A."},{"first_name":"Jenkang","full_name":"Tao, Jenkang","last_name":"Tao"},{"first_name":"Jon M.","full_name":"Resch, Jon M.","last_name":"Resch"},{"first_name":"Bradford B.","full_name":"Lowell, Bradford B.","last_name":"Lowell"}],"date_created":"2026-06-08T09:24:25Z","date_published":"2026-06-03T00:00:00Z","article_type":"original","OA_type":"green","external_id":{"pmid":["42235510"]},"publication_status":"inpress","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"AmDo"}],"publication_identifier":{"issn":["0896-6273"],"eissn":[" 1097-4199"]},"day":"03","main_file_link":[{"url":"https://doi.org/10.1101/2025.09.27.678865","open_access":"1"}],"status":"public","OA_place":"repository","oa":1,"type":"journal_article","citation":{"short":"S.J. Walker, E.D. Lowenstein, A.M. Douglass, C.M.P. Thomas, J.C. Madara, H. Kucukdereli, E.A. Barbosa-Meillon, J. Tao, J.M. Resch, B.B. Lowell, Neuron (n.d.).","apa":"Walker, S. J., Lowenstein, E. D., Douglass, A. M., Thomas, C. M. P., Madara, J. C., Kucukdereli, H., … Lowell, B. B. (n.d.). A hypothalamic circuit for anticipating future changes in energy balance. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2026.05.010\">https://doi.org/10.1016/j.neuron.2026.05.010</a>","chicago":"Walker, Samuel J., Elijah D. Lowenstein, Amelia M. Douglass, Callum M.P. Thomas, Joseph C. Madara, Hakan Kucukdereli, Eunice A. Barbosa-Meillon, Jenkang Tao, Jon M. Resch, and Bradford B. Lowell. “A Hypothalamic Circuit for Anticipating Future Changes in Energy Balance.” <i>Neuron</i>. Elsevier, n.d. <a href=\"https://doi.org/10.1016/j.neuron.2026.05.010\">https://doi.org/10.1016/j.neuron.2026.05.010</a>.","ista":"Walker SJ, Lowenstein ED, Douglass AM, Thomas CMP, Madara JC, Kucukdereli H, Barbosa-Meillon EA, Tao J, Resch JM, Lowell BB. A hypothalamic circuit for anticipating future changes in energy balance. Neuron.","ama":"Walker SJ, Lowenstein ED, Douglass AM, et al. A hypothalamic circuit for anticipating future changes in energy balance. <i>Neuron</i>. doi:<a href=\"https://doi.org/10.1016/j.neuron.2026.05.010\">10.1016/j.neuron.2026.05.010</a>","ieee":"S. J. Walker <i>et al.</i>, “A hypothalamic circuit for anticipating future changes in energy balance,” <i>Neuron</i>. Elsevier.","mla":"Walker, Samuel J., et al. “A Hypothalamic Circuit for Anticipating Future Changes in Energy Balance.” <i>Neuron</i>, Elsevier, doi:<a href=\"https://doi.org/10.1016/j.neuron.2026.05.010\">10.1016/j.neuron.2026.05.010</a>."},"month":"06","keyword":["hunger","hypothalamus","AGRP neurons","neuroscience","metabolism","homeostasis","feeding","food intake","energy balance","appetite"],"_id":"21955","abstract":[{"lang":"eng","text":"AgRP neurons cause hunger, the drive to seek and consume food. Their activation by fasting is key for survival and is thought to be triggered by feedback when energy stores are low. However, we know that environmental cues can also regulate AgRP neurons since cues that predict future food intake rapidly inhibit AgRP neurons, but is the converse true: can the prediction of future fasting rapidly activate AgRP neurons? Here, we show in mice that such rapid fasting activation of AgRP neurons does occur. This rapid activation is driven by excitatory input from paraventricular hypothalamic (PVH) neurons expressing Sim2, which are bidirectionally sensitive to predictions of future energy state. Thus, cognitively processed contextual information conveyed by PVHSim2 neurons strongly activates AgRP neurons. Lastly, chronic silencing of PVHSim2 neurons causes persistent hypophagia. This PVHSim2-to-AgRP-neuron circuit, by anticipating and preventing negative energy balance, provides an important new dimension of hunger regulation."}],"date_updated":"2026-06-16T08:35:11Z","language":[{"iso":"eng"}],"quality_controlled":"1","publisher":"Elsevier","oa_version":"Preprint"},{"OA_type":"closed access","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","extern":"1","publication_status":"published","external_id":{"pmid":["39719709"]},"status":"public","publication_identifier":{"issn":["1550-4131"]},"day":"04","volume":37,"pmid":1,"scopus_import":"1","publication":"Cell Metabolism","year":"2024","intvolume":"        37","doi":"10.1016/j.cmet.2024.11.009","issue":"3","date_created":"2025-04-03T12:27:39Z","author":[{"orcid":"0000-0001-5398-6473","last_name":"Douglass","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","full_name":"Douglass, Amelia May Barnett","first_name":"Amelia May Barnett"},{"first_name":"Hakan","full_name":"Kucukdereli, Hakan","last_name":"Kucukdereli"},{"last_name":"Madara","full_name":"Madara, Joseph C.","first_name":"Joseph C."},{"last_name":"Wang","first_name":"Daqing","full_name":"Wang, Daqing"},{"last_name":"Wu","first_name":"Chen","full_name":"Wu, Chen"},{"full_name":"Lowenstein, Elijah D.","first_name":"Elijah D.","last_name":"Lowenstein"},{"last_name":"Tao","full_name":"Tao, Jenkang","first_name":"Jenkang"},{"last_name":"Lowell","first_name":"Bradford B.","full_name":"Lowell, Bradford B."}],"title":"Acute and circadian feedforward regulation of agouti-related peptide hunger neurons","article_type":"original","date_published":"2024-03-04T00:00:00Z","date_updated":"2025-07-10T11:51:40Z","language":[{"iso":"eng"}],"oa_version":"None","publisher":"Elsevier","quality_controlled":"1","citation":{"ieee":"A. M. Douglass <i>et al.</i>, “Acute and circadian feedforward regulation of agouti-related peptide hunger neurons,” <i>Cell Metabolism</i>, vol. 37, no. 3. Elsevier, p. 708–722.e5, 2024.","mla":"Douglass, Amelia M., et al. “Acute and Circadian Feedforward Regulation of Agouti-Related Peptide Hunger Neurons.” <i>Cell Metabolism</i>, vol. 37, no. 3, Elsevier, 2024, p. 708–722.e5, doi:<a href=\"https://doi.org/10.1016/j.cmet.2024.11.009\">10.1016/j.cmet.2024.11.009</a>.","chicago":"Douglass, Amelia M., Hakan Kucukdereli, Joseph C. Madara, Daqing Wang, Chen Wu, Elijah D. Lowenstein, Jenkang Tao, and Bradford B. Lowell. “Acute and Circadian Feedforward Regulation of Agouti-Related Peptide Hunger Neurons.” <i>Cell Metabolism</i>. Elsevier, 2024. <a href=\"https://doi.org/10.1016/j.cmet.2024.11.009\">https://doi.org/10.1016/j.cmet.2024.11.009</a>.","ista":"Douglass AM, Kucukdereli H, Madara JC, Wang D, Wu C, Lowenstein ED, Tao J, Lowell BB. 2024. Acute and circadian feedforward regulation of agouti-related peptide hunger neurons. Cell Metabolism. 37(3), 708–722.e5.","ama":"Douglass AM, Kucukdereli H, Madara JC, et al. Acute and circadian feedforward regulation of agouti-related peptide hunger neurons. <i>Cell Metabolism</i>. 2024;37(3):708-722.e5. doi:<a href=\"https://doi.org/10.1016/j.cmet.2024.11.009\">10.1016/j.cmet.2024.11.009</a>","short":"A.M. Douglass, H. Kucukdereli, J.C. Madara, D. Wang, C. Wu, E.D. Lowenstein, J. Tao, B.B. Lowell, Cell Metabolism 37 (2024) 708–722.e5.","apa":"Douglass, A. M., Kucukdereli, H., Madara, J. C., Wang, D., Wu, C., Lowenstein, E. D., … Lowell, B. B. (2024). Acute and circadian feedforward regulation of agouti-related peptide hunger neurons. <i>Cell Metabolism</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cmet.2024.11.009\">https://doi.org/10.1016/j.cmet.2024.11.009</a>"},"month":"03","type":"journal_article","page":"708-722.e5","abstract":[{"lang":"eng","text":"When food is freely available, eating occurs without energy deficit. While agouti-related peptide (AgRP) neurons are likely involved, their activation is thought to require negative energy balance. To investigate this, we implemented long-term, continuous in vivo fiber-photometry recordings in mice. We discovered new forms of AgRP neuron regulation, including fast pre-ingestive decreases in activity and unexpectedly rapid activation by fasting. Furthermore, AgRP neuron activity has a circadian rhythm that peaks concurrent with the daily feeding onset. Importantly, this rhythm persists when nutrition is provided via constant-rate gastric infusions. Hence, it is not secondary to a circadian feeding rhythm. The AgRP neuron rhythm is driven by the circadian clock, the suprachiasmatic nucleus (SCN), as SCN ablation abolishes the circadian rhythm in AgRP neuron activity and feeding. The SCN activates AgRP neurons via excitatory afferents from thyrotrophin-releasing hormone-expressing neurons in the dorsomedial hypothalamus (DMHTrh neurons) to drive daily feeding rhythms."}],"_id":"19470"},{"OA_type":"green","main_file_link":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC11168300/","open_access":"1"}],"status":"public","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"day":"03","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_status":"published","extern":"1","external_id":{"pmid":["37495689 "]},"intvolume":"       620","doi":"10.1038/s41586-023-06358-0","volume":620,"pmid":1,"scopus_import":"1","publication":"Nature","year":"2023","article_type":"original","date_published":"2023-08-03T00:00:00Z","issue":"7972","date_created":"2025-04-03T12:28:51Z","author":[{"full_name":"Douglass, Amelia May Barnett","first_name":"Amelia May Barnett","orcid":"0000-0001-5398-6473","last_name":"Douglass","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289"},{"last_name":"Resch","full_name":"Resch, Jon M.","first_name":"Jon M."},{"first_name":"Joseph C.","full_name":"Madara, Joseph C.","last_name":"Madara"},{"last_name":"Kucukdereli","first_name":"Hakan","full_name":"Kucukdereli, Hakan"},{"full_name":"Yizhar, Ofer","first_name":"Ofer","last_name":"Yizhar"},{"last_name":"Grama","first_name":"Abhinav","full_name":"Grama, Abhinav"},{"last_name":"Yamagata","first_name":"Masahito","full_name":"Yamagata, Masahito"},{"last_name":"Yang","full_name":"Yang, Zongfang","first_name":"Zongfang"},{"first_name":"Bradford B.","full_name":"Lowell, Bradford B.","last_name":"Lowell"}],"title":"Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis","oa_version":"Submitted Version","publisher":"Springer Nature","quality_controlled":"1","language":[{"iso":"eng"}],"date_updated":"2025-07-10T11:51:40Z","OA_place":"repository","abstract":[{"text":"Fasting initiates a multitude of adaptations to allow survival. Activation of the hypothalamic–pituitary–adrenal (HPA) axis and subsequent release of glucocorticoid hormones is a key response that mobilizes fuel stores to meet energy demands1,2,3,4,5. Despite the importance of the HPA axis response, the neural mechanisms that drive its activation during energy deficit are unknown. Here, we show that fasting-activated hypothalamic agouti-related peptide (AgRP)-expressing neurons trigger and are essential for fasting-induced HPA axis activation. AgRP neurons do so through projections to the paraventricular hypothalamus (PVH), where, in a mechanism not previously described for AgRP neurons, they presynaptically inhibit the terminals of tonically active GABAergic afferents from the bed nucleus of the stria terminalis (BNST) that otherwise restrain activity of corticotrophin-releasing hormone (CRH)-expressing neurons. This disinhibition of PVHCrh neurons requires γ-aminobutyric acid (GABA)/GABA-B receptor signalling and potently activates the HPA axis. Notably, stimulation of the HPA axis by AgRP neurons is independent of their induction of hunger, showing that these canonical ‘hunger neurons’ drive many distinctly different adaptations to the fasted state. Together, our findings identify the neural basis for fasting-induced HPA axis activation and uncover a unique means by which AgRP neurons activate downstream neurons: through presynaptic inhibition of GABAergic afferents. Given the potency of this disinhibition of tonically active BNST afferents, other activators of the HPA axis, such as psychological stress, may also work by reducing BNST inhibitory tone onto PVHCrh neurons.","lang":"eng"}],"_id":"19471","citation":{"ama":"Douglass AM, Resch JM, Madara JC, et al. Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis. <i>Nature</i>. 2023;620(7972):154-162. doi:<a href=\"https://doi.org/10.1038/s41586-023-06358-0\">10.1038/s41586-023-06358-0</a>","ista":"Douglass AM, Resch JM, Madara JC, Kucukdereli H, Yizhar O, Grama A, Yamagata M, Yang Z, Lowell BB. 2023. Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis. Nature. 620(7972), 154–162.","chicago":"Douglass, Amelia M., Jon M. Resch, Joseph C. Madara, Hakan Kucukdereli, Ofer Yizhar, Abhinav Grama, Masahito Yamagata, Zongfang Yang, and Bradford B. Lowell. “Neural Basis for Fasting Activation of the Hypothalamic–Pituitary–Adrenal Axis.” <i>Nature</i>. Springer Nature, 2023. <a href=\"https://doi.org/10.1038/s41586-023-06358-0\">https://doi.org/10.1038/s41586-023-06358-0</a>.","short":"A.M. Douglass, J.M. Resch, J.C. Madara, H. Kucukdereli, O. Yizhar, A. Grama, M. Yamagata, Z. Yang, B.B. Lowell, Nature 620 (2023) 154–162.","apa":"Douglass, A. M., Resch, J. M., Madara, J. C., Kucukdereli, H., Yizhar, O., Grama, A., … Lowell, B. B. (2023). Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41586-023-06358-0\">https://doi.org/10.1038/s41586-023-06358-0</a>","ieee":"A. M. Douglass <i>et al.</i>, “Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis,” <i>Nature</i>, vol. 620, no. 7972. Springer Nature, pp. 154–162, 2023.","mla":"Douglass, Amelia M., et al. “Neural Basis for Fasting Activation of the Hypothalamic–Pituitary–Adrenal Axis.” <i>Nature</i>, vol. 620, no. 7972, Springer Nature, 2023, pp. 154–62, doi:<a href=\"https://doi.org/10.1038/s41586-023-06358-0\">10.1038/s41586-023-06358-0</a>."},"type":"journal_article","month":"08","page":"154-162","oa":1},{"title":"DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation","author":[{"last_name":"Morcom","full_name":"Morcom, Laura","first_name":"Laura"},{"full_name":"Gobius, Ilan","first_name":"Ilan","last_name":"Gobius"},{"last_name":"Marsh","full_name":"Marsh, Ashley PL","first_name":"Ashley PL"},{"full_name":"Suárez, Rodrigo","first_name":"Rodrigo","last_name":"Suárez"},{"last_name":"Lim","first_name":"Jonathan WC","full_name":"Lim, Jonathan WC"},{"full_name":"Bridges, Caitlin","first_name":"Caitlin","last_name":"Bridges"},{"first_name":"Yunan","full_name":"Ye, Yunan","last_name":"Ye"},{"last_name":"Fenlon","first_name":"Laura R","full_name":"Fenlon, Laura R"},{"full_name":"Zagar, Yvrick","first_name":"Yvrick","last_name":"Zagar"},{"last_name":"Douglass","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","orcid":"0000-0001-5398-6473","first_name":"Amelia May Barnett","full_name":"Douglass, Amelia May Barnett"},{"last_name":"Donahoo","first_name":"Amber-Lee S","full_name":"Donahoo, Amber-Lee S"},{"last_name":"Fothergill","first_name":"Thomas","full_name":"Fothergill, Thomas"},{"last_name":"Shaikh","first_name":"Samreen","full_name":"Shaikh, Samreen"},{"last_name":"Kozulin","first_name":"Peter","full_name":"Kozulin, Peter"},{"full_name":"Edwards, Timothy J","first_name":"Timothy J","last_name":"Edwards"},{"last_name":"Cooper","first_name":"Helen M","full_name":"Cooper, Helen M"},{"last_name":"Sherr","first_name":"Elliott H","full_name":"Sherr, Elliott H"},{"first_name":"Alain","full_name":"Chédotal, Alain","last_name":"Chédotal"},{"last_name":"Leventer","full_name":"Leventer, Richard J","first_name":"Richard J"},{"last_name":"Lockhart","full_name":"Lockhart, Paul J","first_name":"Paul J"},{"full_name":"Richards, Linda J","first_name":"Linda J","last_name":"Richards"}],"date_created":"2025-04-03T12:29:29Z","article_number":"61769","date_published":"2021-04-19T00:00:00Z","article_type":"original","scopus_import":"1","pmid":1,"publication":"eLife","year":"2021","volume":10,"doi":"10.7554/elife.61769","intvolume":"        10","publication_status":"published","extern":"1","external_id":{"pmid":["33871356"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes","day":"19","publication_identifier":{"eissn":["2050-084X"]},"status":"public","has_accepted_license":"1","main_file_link":[{"url":"https://doi.org/10.7554/eLife.61769","open_access":"1"}],"OA_type":"gold","oa":1,"month":"04","type":"journal_article","citation":{"mla":"Morcom, Laura, et al. “DCC Regulates Astroglial Development Essential for Telencephalic Morphogenesis and Corpus Callosum Formation.” <i>ELife</i>, vol. 10, 61769, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.61769\">10.7554/elife.61769</a>.","ieee":"L. Morcom <i>et al.</i>, “DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","short":"L. Morcom, I. Gobius, A.P. Marsh, R. Suárez, J.W. Lim, C. Bridges, Y. Ye, L.R. Fenlon, Y. Zagar, A.M. Douglass, A.-L.S. Donahoo, T. Fothergill, S. Shaikh, P. Kozulin, T.J. Edwards, H.M. Cooper, E.H. Sherr, A. Chédotal, R.J. Leventer, P.J. Lockhart, L.J. Richards, ELife 10 (2021).","apa":"Morcom, L., Gobius, I., Marsh, A. P., Suárez, R., Lim, J. W., Bridges, C., … Richards, L. J. (2021). DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.61769\">https://doi.org/10.7554/elife.61769</a>","ista":"Morcom L, Gobius I, Marsh AP, Suárez R, Lim JW, Bridges C, Ye Y, Fenlon LR, Zagar Y, Douglass AM, Donahoo A-LS, Fothergill T, Shaikh S, Kozulin P, Edwards TJ, Cooper HM, Sherr EH, Chédotal A, Leventer RJ, Lockhart PJ, Richards LJ. 2021. DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. eLife. 10, 61769.","chicago":"Morcom, Laura, Ilan Gobius, Ashley PL Marsh, Rodrigo Suárez, Jonathan WC Lim, Caitlin Bridges, Yunan Ye, et al. “DCC Regulates Astroglial Development Essential for Telencephalic Morphogenesis and Corpus Callosum Formation.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.61769\">https://doi.org/10.7554/elife.61769</a>.","ama":"Morcom L, Gobius I, Marsh AP, et al. DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.61769\">10.7554/elife.61769</a>"},"_id":"19472","abstract":[{"lang":"eng","text":"The forebrain hemispheres are predominantly separated during embryogenesis by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form a continuous substrate between the hemispheres for midline crossing of the corpus callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma (DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved function in commissural axon guidance. The CC and HC are absent in <jats:italic>Dcc</jats:italic> and <jats:italic>Ntn1</jats:italic> knockout mice, while other commissures are only partially affected, suggesting an additional aetiology in forebrain commissure formation. Here, we find that these molecules play a critical role in regulating astroglial development and IHF remodelling during CC and HC formation. Human subjects with <jats:italic>DCC</jats:italic> mutations display disrupted IHF remodelling associated with CC and HC malformations. Thus, axon guidance molecules such as DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures prior to their role in regulating axonal growth and guidance across it."}],"license":"https://creativecommons.org/licenses/by/4.0/","OA_place":"publisher","DOAJ_listed":"1","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"date_updated":"2025-07-10T11:51:41Z","language":[{"iso":"eng"}],"publisher":"eLife Sciences Publications","quality_controlled":"1","oa_version":"Published Version"},{"quality_controlled":"1","publisher":"National Academy of Sciences","oa_version":"Published Version","date_updated":"2025-07-10T11:51:42Z","language":[{"iso":"eng"}],"tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"OA_place":"publisher","_id":"19473","abstract":[{"lang":"eng","text":"Leptin informs the brain about sufficiency of fuel stores. When insufficient, leptin levels fall, triggering compensatory increases in appetite. Falling leptin is first sensed by hypothalamic neurons, which then initiate adaptive responses. With regard to hunger, it is thought that leptin-sensing neurons work entirely via circuits within the central nervous system (CNS). Very unexpectedly, however, we now show this is not the case. Instead, stimulation of hunger requires an intervening endocrine step, namely activation of the hypothalamic–pituitary–adrenocortical (HPA) axis. Increased corticosterone then activates AgRP neurons to fully increase hunger. Importantly, this is true for 2 forms of low leptin-induced hunger, fasting and poorly controlled type 1 diabetes. Hypoglycemia, which also stimulates hunger by activating CNS neurons, albeit independently of leptin, similarly recruits and requires this pathway by which HPA axis activity stimulates AgRP neurons. Thus, HPA axis regulation of AgRP neurons is a previously underappreciated step in homeostatic regulation of hunger."}],"oa":1,"page":"13670-13679","month":"07","type":"journal_article","citation":{"ama":"Perry RJ, Resch JM, Douglass AM, et al. Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. <i>Proceedings of the National Academy of Sciences</i>. 2019;116(27):13670-13679. doi:<a href=\"https://doi.org/10.1073/pnas.1901795116\">10.1073/pnas.1901795116</a>","chicago":"Perry, Rachel J., Jon M. Resch, Amelia M. Douglass, Joseph C. Madara, Aviva Rabin-Court, Hakan Kucukdereli, Chen Wu, Joongyu D. Song, Bradford B. Lowell, and Gerald I. Shulman. “Leptin’s Hunger-Suppressing Effects Are Mediated by the Hypothalamic–Pituitary–Adrenocortical Axis in Rodents.” <i>Proceedings of the National Academy of Sciences</i>. National Academy of Sciences, 2019. <a href=\"https://doi.org/10.1073/pnas.1901795116\">https://doi.org/10.1073/pnas.1901795116</a>.","ista":"Perry RJ, Resch JM, Douglass AM, Madara JC, Rabin-Court A, Kucukdereli H, Wu C, Song JD, Lowell BB, Shulman GI. 2019. Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. Proceedings of the National Academy of Sciences. 116(27), 13670–13679.","short":"R.J. Perry, J.M. Resch, A.M. Douglass, J.C. Madara, A. Rabin-Court, H. Kucukdereli, C. Wu, J.D. Song, B.B. Lowell, G.I. Shulman, Proceedings of the National Academy of Sciences 116 (2019) 13670–13679.","apa":"Perry, R. J., Resch, J. M., Douglass, A. M., Madara, J. C., Rabin-Court, A., Kucukdereli, H., … Shulman, G. I. (2019). Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. <i>Proceedings of the National Academy of Sciences</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1901795116\">https://doi.org/10.1073/pnas.1901795116</a>","ieee":"R. J. Perry <i>et al.</i>, “Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents,” <i>Proceedings of the National Academy of Sciences</i>, vol. 116, no. 27. National Academy of Sciences, pp. 13670–13679, 2019.","mla":"Perry, Rachel J., et al. “Leptin’s Hunger-Suppressing Effects Are Mediated by the Hypothalamic–Pituitary–Adrenocortical Axis in Rodents.” <i>Proceedings of the National Academy of Sciences</i>, vol. 116, no. 27, National Academy of Sciences, 2019, pp. 13670–79, doi:<a href=\"https://doi.org/10.1073/pnas.1901795116\">10.1073/pnas.1901795116</a>."},"OA_type":"hybrid","publication_identifier":{"eissn":["1091-6490"],"issn":["0027-8424"]},"day":"02","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1073/pnas.1901795116"}],"has_accepted_license":"1","status":"public","external_id":{"pmid":["31213533"]},"publication_status":"published","extern":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes (in subscription journal)","ddc":["570"],"doi":"10.1073/pnas.1901795116","intvolume":"       116","publication":"Proceedings of the National Academy of Sciences","year":"2019","scopus_import":"1","pmid":1,"volume":116,"date_published":"2019-07-02T00:00:00Z","article_type":"original","date_created":"2025-04-03T12:30:19Z","title":"Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents","author":[{"first_name":"Rachel J.","full_name":"Perry, Rachel J.","last_name":"Perry"},{"last_name":"Resch","full_name":"Resch, Jon M.","first_name":"Jon M."},{"first_name":"Amelia May Barnett","full_name":"Douglass, Amelia May Barnett","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","last_name":"Douglass","orcid":"0000-0001-5398-6473"},{"last_name":"Madara","first_name":"Joseph C.","full_name":"Madara, Joseph C."},{"first_name":"Aviva","full_name":"Rabin-Court, Aviva","last_name":"Rabin-Court"},{"last_name":"Kucukdereli","full_name":"Kucukdereli, Hakan","first_name":"Hakan"},{"full_name":"Wu, Chen","first_name":"Chen","last_name":"Wu"},{"full_name":"Song, Joongyu D.","first_name":"Joongyu D.","last_name":"Song"},{"last_name":"Lowell","full_name":"Lowell, Bradford B.","first_name":"Bradford B."},{"last_name":"Shulman","full_name":"Shulman, Gerald I.","first_name":"Gerald I."}],"issue":"27"},{"volume":20,"year":"2017","publication":"Nature Neuroscience","pmid":1,"scopus_import":"1","intvolume":"        20","doi":"10.1038/nn.4623","issue":"10","title":"Central amygdala circuits modulate food consumption through a positive-valence mechanism","author":[{"first_name":"Amelia May Barnett","full_name":"Douglass, Amelia May Barnett","last_name":"Douglass","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","orcid":"0000-0001-5398-6473"},{"last_name":"Kucukdereli","first_name":"Hakan","full_name":"Kucukdereli, Hakan"},{"full_name":"Ponserre, Marion","first_name":"Marion","last_name":"Ponserre"},{"last_name":"Markovic","full_name":"Markovic, Milica","first_name":"Milica"},{"full_name":"Gründemann, Jan","first_name":"Jan","last_name":"Gründemann"},{"first_name":"Cornelia","full_name":"Strobel, Cornelia","last_name":"Strobel"},{"full_name":"Alcala Morales, Pilar L","first_name":"Pilar L","last_name":"Alcala Morales"},{"last_name":"Conzelmann","full_name":"Conzelmann, Karl-Klaus","first_name":"Karl-Klaus"},{"full_name":"Lüthi, Andreas","first_name":"Andreas","last_name":"Lüthi"},{"full_name":"Klein, Rüdiger","first_name":"Rüdiger","last_name":"Klein"}],"date_created":"2025-04-03T12:30:57Z","article_type":"original","date_published":"2017-10-01T00:00:00Z","OA_type":"green","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","external_id":{"pmid":["28825719 "]},"extern":"1","publication_status":"published","main_file_link":[{"url":"https://doi.org/10.1101/145375","open_access":"1"}],"status":"public","publication_identifier":{"issn":["1097-6256"],"eissn":["1546-1726"]},"day":"01","OA_place":"repository","month":"10","type":"journal_article","citation":{"ama":"Douglass AM, Kucukdereli H, Ponserre M, et al. Central amygdala circuits modulate food consumption through a positive-valence mechanism. <i>Nature Neuroscience</i>. 2017;20(10):1384-1394. doi:<a href=\"https://doi.org/10.1038/nn.4623\">10.1038/nn.4623</a>","ista":"Douglass AM, Kucukdereli H, Ponserre M, Markovic M, Gründemann J, Strobel C, Alcala Morales PL, Conzelmann K-K, Lüthi A, Klein R. 2017. Central amygdala circuits modulate food consumption through a positive-valence mechanism. Nature Neuroscience. 20(10), 1384–1394.","chicago":"Douglass, Amelia M., Hakan Kucukdereli, Marion Ponserre, Milica Markovic, Jan Gründemann, Cornelia Strobel, Pilar L Alcala Morales, Karl-Klaus Conzelmann, Andreas Lüthi, and Rüdiger Klein. “Central Amygdala Circuits Modulate Food Consumption through a Positive-Valence Mechanism.” <i>Nature Neuroscience</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/nn.4623\">https://doi.org/10.1038/nn.4623</a>.","short":"A.M. Douglass, H. Kucukdereli, M. Ponserre, M. Markovic, J. Gründemann, C. Strobel, P.L. Alcala Morales, K.-K. Conzelmann, A. Lüthi, R. Klein, Nature Neuroscience 20 (2017) 1384–1394.","apa":"Douglass, A. M., Kucukdereli, H., Ponserre, M., Markovic, M., Gründemann, J., Strobel, C., … Klein, R. (2017). Central amygdala circuits modulate food consumption through a positive-valence mechanism. <i>Nature Neuroscience</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nn.4623\">https://doi.org/10.1038/nn.4623</a>","ieee":"A. M. Douglass <i>et al.</i>, “Central amygdala circuits modulate food consumption through a positive-valence mechanism,” <i>Nature Neuroscience</i>, vol. 20, no. 10. Springer Nature, pp. 1384–1394, 2017.","mla":"Douglass, Amelia M., et al. “Central Amygdala Circuits Modulate Food Consumption through a Positive-Valence Mechanism.” <i>Nature Neuroscience</i>, vol. 20, no. 10, Springer Nature, 2017, pp. 1384–94, doi:<a href=\"https://doi.org/10.1038/nn.4623\">10.1038/nn.4623</a>."},"oa":1,"page":"1384-1394","abstract":[{"lang":"eng","text":"The complex behaviors underlying reward seeking and consumption are integral to organism survival. The hypothalamus and mesolimbic dopamine system are key mediators of these behaviors, yet regulation of appetitive and consummatory behaviors outside of these regions is poorly understood. The central nucleus of the amygdala (CeA) has been implicated in feeding and reward, but the neurons and circuit mechanisms that positively regulate these behaviors remain unclear. Here, we defined the neuronal mechanisms by which CeA neurons promote food consumption. Using in vivo activity manipulations and Ca2+ imaging in mice, we found that GABAergic serotonin receptor 2a (Htr2a)-expressing CeA neurons modulate food consumption, promote positive reinforcement and are active in vivo during eating. We demonstrated electrophysiologically, anatomically and behaviorally that intra-CeA and long-range circuit mechanisms underlie these behaviors. Finally, we showed that CeAHtr2a neurons receive inputs from feeding-relevant brain regions. Our results illustrate how defined CeA neural circuits positively regulate food consumption."}],"_id":"19474","date_updated":"2025-07-10T11:51:42Z","language":[{"iso":"eng"}],"oa_version":"Preprint","quality_controlled":"1","publisher":"Springer Nature"},{"publication_identifier":{"eissn":["1460-2199"],"issn":["1047-3211"]},"day":"01","status":"public","external_id":{"pmid":["23302812 "]},"publication_status":"published","extern":"1","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","OA_type":"closed access","date_published":"2014-05-01T00:00:00Z","article_type":"original","date_created":"2025-04-03T12:31:58Z","title":"Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion","author":[{"last_name":"Fothergill","first_name":"Thomas","full_name":"Fothergill, Thomas"},{"last_name":"Donahoo","first_name":"Amber-Lee S.","full_name":"Donahoo, Amber-Lee S."},{"orcid":"0000-0001-5398-6473","id":"de5f6fda-80fb-11ef-996f-a8c4ecd8e289","last_name":"Douglass","full_name":"Douglass, Amelia May Barnett","first_name":"Amelia May Barnett"},{"first_name":"Oressia","full_name":"Zalucki, Oressia","last_name":"Zalucki"},{"full_name":"Yuan, Jiajia","first_name":"Jiajia","last_name":"Yuan"},{"last_name":"Shu","first_name":"Tianzhi","full_name":"Shu, Tianzhi"},{"full_name":"Goodhill, Geoffrey J.","first_name":"Geoffrey J.","last_name":"Goodhill"},{"full_name":"Richards, Linda J.","first_name":"Linda J.","last_name":"Richards"}],"issue":"5","doi":"10.1093/cercor/bhs395","intvolume":"        24","publication":"Cerebral Cortex","year":"2014","scopus_import":"1","pmid":1,"volume":24,"quality_controlled":"1","publisher":"Oxford University Press","oa_version":"None","date_updated":"2025-07-10T11:51:43Z","language":[{"iso":"eng"}],"_id":"19475","abstract":[{"lang":"eng","text":"The left and right sides of the nervous system communicate via commissural axons that cross the midline during development using evolutionarily conserved molecules. These guidance cues have been particularly well studied in the mammalian spinal cord, but it remains unclear whether these guidance mechanisms for commissural axons are similar in the developing forebrain, in particular for the corpus callosum, the largest and most important commissure for cortical function. Here, we show that Netrin1 initially attracts callosal pioneering axons derived from the cingulate cortex, but surprisingly is not attractive for the neocortical callosal axons that make up the bulk of the projection. Instead, we show that Netrin-deleted in colorectal cancer signaling acts in a fundamentally different manner, to prevent the Slit2-mediated repulsion of precrossing axons thereby allowing them to approach and cross the midline. These results provide the first evidence for how callosal axons integrate multiple guidance cues to navigate the midline."}],"page":"1138-1151","type":"journal_article","citation":{"mla":"Fothergill, Thomas, et al. “Netrin-DCC Signaling Regulates Corpus Callosum Formation through Attraction of Pioneering Axons and by Modulating Slit2-Mediated Repulsion.” <i>Cerebral Cortex</i>, vol. 24, no. 5, Oxford University Press, 2014, pp. 1138–51, doi:<a href=\"https://doi.org/10.1093/cercor/bhs395\">10.1093/cercor/bhs395</a>.","ieee":"T. Fothergill <i>et al.</i>, “Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion,” <i>Cerebral Cortex</i>, vol. 24, no. 5. Oxford University Press, pp. 1138–1151, 2014.","short":"T. Fothergill, A.-L.S. Donahoo, A.M. Douglass, O. Zalucki, J. Yuan, T. Shu, G.J. Goodhill, L.J. Richards, Cerebral Cortex 24 (2014) 1138–1151.","apa":"Fothergill, T., Donahoo, A.-L. S., Douglass, A. M., Zalucki, O., Yuan, J., Shu, T., … Richards, L. J. (2014). Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion. <i>Cerebral Cortex</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/cercor/bhs395\">https://doi.org/10.1093/cercor/bhs395</a>","ista":"Fothergill T, Donahoo A-LS, Douglass AM, Zalucki O, Yuan J, Shu T, Goodhill GJ, Richards LJ. 2014. Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion. Cerebral Cortex. 24(5), 1138–1151.","chicago":"Fothergill, Thomas, Amber-Lee S. Donahoo, Amelia M. Douglass, Oressia Zalucki, Jiajia Yuan, Tianzhi Shu, Geoffrey J. Goodhill, and Linda J. Richards. “Netrin-DCC Signaling Regulates Corpus Callosum Formation through Attraction of Pioneering Axons and by Modulating Slit2-Mediated Repulsion.” <i>Cerebral Cortex</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/cercor/bhs395\">https://doi.org/10.1093/cercor/bhs395</a>.","ama":"Fothergill T, Donahoo A-LS, Douglass AM, et al. Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion. <i>Cerebral Cortex</i>. 2014;24(5):1138-1151. doi:<a href=\"https://doi.org/10.1093/cercor/bhs395\">10.1093/cercor/bhs395</a>"},"month":"05"}]