Adaptation to photoperiod via dynamic neurotransmitter segregation.

Autor: Maddaloni G; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA., Chang YJ; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA., Senft RA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA., Dymecki SM; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA. dymecki@genetics.med.harvard.edu.
Jazyk: angličtina
Zdroj: Nature [Nature] 2024 Aug; Vol. 632 (8023), pp. 147-156. Date of Electronic Publication: 2024 Jul 17.
DOI: 10.1038/s41586-024-07692-7
Abstrakt: Changes in the amount of daylight (photoperiod) alter physiology and behaviour 1,2 . Adaptive responses to seasonal photoperiods are vital to all organisms-dysregulation associates with disease, including affective disorders 3 and metabolic syndromes 4 . The circadian rhythm circuitry is implicated in such responses 5,6 , yet little is known about the precise cellular substrates that underlie phase synchronization to photoperiod change. Here we identify a brain circuit and system of axon branch-specific and reversible neurotransmitter deployment that are critical for behavioural and sleep adaptation to photoperiod. A type of neuron called mrEn1-Pet1 7 in the mouse brainstem median raphe nucleus segregates serotonin from VGLUT3 (also known as SLC17A8, a proxy for glutamate) to different axonal branches that innervate specific brain regions involved in circadian rhythm and sleep-wake timing 8,9 . This branch-specific neurotransmitter deployment did not distinguish between daylight and dark phase; however, it reorganized with change in photoperiod. Axonal boutons, but not cell soma, changed neurochemical phenotype upon a shift away from equinox light/dark conditions, and these changes were reversed upon return to equinox conditions. When we genetically disabled Vglut3 in mrEn1-Pet1 neurons, sleep-wake periods, voluntary activity and clock gene expression did not synchronize to the new photoperiod or were delayed. Combining intersectional rabies virus tracing and projection-specific neuronal silencing, we delineated a preoptic area-to-mrEn1Pet1 connection that was responsible for decoding the photoperiodic inputs, driving the neurotransmitter reorganization and promoting behavioural synchronization. Our results reveal a brain circuit and periodic, branch-specific neurotransmitter deployment that regulates organismal adaptation to photoperiod change.
(© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)
Databáze: MEDLINE
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