Orexin-driven GAD65 network of the lateral hypothalamus sets physical activity in mice
Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 114; no. 17; pp. 4525 - 4530 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
25.04.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.1619700114 |
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| Abstract | Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65LH neurons. We demonstrate that internally initiated GAD65LH cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65LH cell activity depresses voluntary locomotion, and that GAD65LH cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. |
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| AbstractList | Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65LH neurons. We demonstrate that internally initiated GAD65LH cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65LH cell activity depresses voluntary locomotion, and that GAD65LH cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice.Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65LH neurons. We demonstrate that internally initiated GAD65LH cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65LH cell activity depresses voluntary locomotion, and that GAD65LH cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. A century ago, it was noted that damage to the lateral hypothalamic (LH) brain area caused people to be motionless most of the time. Therefore, it is thought that this brain area emits essential signals for promoting physical activity. However, it remained a mystery what these signals are. Using newly developed genetic and deep-brain recording methods, we found that, unexpectedly, a critical signal for movement comes from a subset of LH cells that are molecularly distinct from neurons previously implicated in locomotion control. These movement-promoting cells were switched on by the local peptide orexin, a key signal of stress and hunger. These findings shed new light on deep-brain signals that maintain healthy levels of physical activity. Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65 LH neurons. We demonstrate that internally initiated GAD65 LH cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65 LH cell activity depresses voluntary locomotion, and that GAD65 LH cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65 neurons. We demonstrate that internally initiated GAD65 cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65 cell activity depresses voluntary locomotion, and that GAD65 cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65LH neurons. We demonstrate that internally initiated GAD65LH cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65LH cell activity depresses voluntary locomotion, and that GAD65LH cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their interplay in orchestrating physical activity is not fully understood. Here, using optogenetic circuit analysis and cell type-specific deep-brain recordings in behaving mice, we show that orexin cell activation rapidly recruits GAD65^sub LH^ neurons. We demonstrate that internally initiated GAD65^sub LH^ cell bursts precede and accompany spontaneous running bouts, that selective chemogenetic silencing of natural GAD65LH cell activity depresses voluntary locomotion, and that GAD65^sub LH^ cell overactivation leads to hyperlocomotion. These results thus identify a molecularly distinct, orexin-activated LH submodule that governs physical activity in mice. |
| Author | Bracey, Edward Burdakov, Denis Schöne, Cornelia Kosse, Christin |
| Author_xml | – sequence: 1 givenname: Christin surname: Kosse fullname: Kosse, Christin organization: The Francis Crick Institute, London NW1 1AT, United Kingdom – sequence: 2 givenname: Cornelia surname: Schöne fullname: Schöne, Cornelia organization: Centre for Experimental Neurology, Inselspital University Hospital, Bern 3010, Switzerland – sequence: 3 givenname: Edward surname: Bracey fullname: Bracey, Edward organization: The Francis Crick Institute, London NW1 1AT, United Kingdom – sequence: 4 givenname: Denis surname: Burdakov fullname: Burdakov, Denis organization: The Francis Crick Institute, London NW1 1AT, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28396414$$D View this record in MEDLINE/PubMed |
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| Keywords | hypocretin stress orexin GAD65 hypothalamus locomotion |
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| Snippet | Damage to the lateral hypothalamus (LH) causes profound physical inactivity in mammals. Several molecularly distinct types of LH neurons have been identified,... A century ago, it was noted that damage to the lateral hypothalamic (LH) brain area caused people to be motionless most of the time. Therefore, it is thought... |
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| SubjectTerms | Animals Biological Sciences Brain Bursts Cell activation Cells Electrocardiography Exercise Gene Transfer Techniques Glutamate decarboxylase Glutamate Decarboxylase - genetics Glutamate Decarboxylase - metabolism Glutamic acid Hypothalamic Area, Lateral - physiology Hypothalamus Hypothalamus (lateral) Locomotion Luteinizing hormone Male Mice Motor Activity - physiology Neurons Orexins Orexins - physiology Physical activity Rodents |
| Title | Orexin-driven GAD65 network of the lateral hypothalamus sets physical activity in mice |
| URI | https://www.jstor.org/stable/26480773 https://www.ncbi.nlm.nih.gov/pubmed/28396414 https://www.proquest.com/docview/1902095721 https://www.proquest.com/docview/1886751435 https://pubmed.ncbi.nlm.nih.gov/PMC5410789 |
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