Journal
CURRENT BIOLOGY
Volume 28, Issue 4, Pages 580-+Publisher
CELL PRESS
DOI: 10.1016/j.cub.2017.12.050
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Funding
- Medical Research Council, UK [G0901892]
- BBSRC [BB/K018159/1]
- BBSRC doctoral training grant [BB/F017324/1]
- Imperial College Schrodinger Scholarship
- European Hematology Association
- Funds for International Cooperation and Exchange of the National Natural Science Foundation of China [81620108012]
- UK Dementia Research Institute
- Wellcome Trust [107839/Z/15/Z, 107841/Z/15/Z]
- Wellcome Trust [107839/Z/15/Z] Funding Source: Wellcome Trust
- BBSRC [BB/K018159/1] Funding Source: UKRI
- MRC [UKDRI-5004, G0901892] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K018159/1, 1100129] Funding Source: researchfish
- Medical Research Council [UKDRI-5004, G0901892] Funding Source: researchfish
- Wellcome Trust [107839/Z/15/Z] Funding Source: researchfish
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The lateral habenula has been widely studied for its contribution in generating reward-related behaviors [1, 2]. We have found that this nucleus plays an unexpected role in the sedative actions of the general anesthetic propofol. The lateral habenula is a gluta-matergic, excitatory hub that projects to multiple targets throughout the brain, including GABAergic and aminergic nuclei that control arousal [3-5]. When glutamate release from the lateral habenula in mice was genetically blocked, the ability of propofol to induce sedation was greatly diminished. In addition to this reduced sensitivity to propofol, blocking output from the lateral habenula caused natural non-rapid eye movement (NREM) sleep to become highly fragmented, especially during the rest (lights on'') period. This fragmentation was largely reversed by the dual orexinergic antagonist almorexant. We conclude that the glutamatergic output from the lateral habenula is permissive for the sedative actions of propofol and is also necessary for the consolidation of natural sleep.
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