TY - JOUR
T1 - Neuromedin s-producing neurons act as essential pacemakers in the suprachiasmatic nucleus to couple clock neurons and dictate circadian rhythms
AU - Lee, Ivan T.
AU - Chang, Alexander S.
AU - Manandhar, Manabu
AU - Shan, Yongli
AU - Fan, Junmei
AU - Izumo, Mariko
AU - Ikeda, Yuichi
AU - Motoike, Toshiyuki
AU - Dixon, Shelley
AU - Seinfeld, Jeffrey E.
AU - Takahashi, Joseph S.
AU - Yanagisawa, Masashi
N1 - Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/3/4
Y1 - 2015/3/4
N2 - Circadian behavior in mammals is orchestrated by neurons within the suprachiasmatic nucleus (SCN), yet the neuronal population necessary for the generation of timekeeping remains unknown. We show that a subset of SCN neurons expressing the neuropeptide neuromedin S (NMS) plays an essential role in the generation of daily rhythms in behavior. We demonstrate that lengthening period within Nms neurons issufficient to lengthen period of the SCN and behavioral circadian rhythms. Conversely, mice without a functional molecular clock within Nms neurons lack synchronous molecular oscillations and coherent behavioral daily rhythms. Interestingly, we found that mice lacking Nms and its closely related paralog, Nmu, do not lose invivo circadian rhythms. However, blocking vesicular transmission from Nms neurons with intact cell-autonomous clocks disrupts the timing mechanisms of the SCN, revealing that Nms neurons define a subpopulation of pacemakers that control SCN network synchrony and invivo circadian rhythms through intercellular synaptic transmission.
AB - Circadian behavior in mammals is orchestrated by neurons within the suprachiasmatic nucleus (SCN), yet the neuronal population necessary for the generation of timekeeping remains unknown. We show that a subset of SCN neurons expressing the neuropeptide neuromedin S (NMS) plays an essential role in the generation of daily rhythms in behavior. We demonstrate that lengthening period within Nms neurons issufficient to lengthen period of the SCN and behavioral circadian rhythms. Conversely, mice without a functional molecular clock within Nms neurons lack synchronous molecular oscillations and coherent behavioral daily rhythms. Interestingly, we found that mice lacking Nms and its closely related paralog, Nmu, do not lose invivo circadian rhythms. However, blocking vesicular transmission from Nms neurons with intact cell-autonomous clocks disrupts the timing mechanisms of the SCN, revealing that Nms neurons define a subpopulation of pacemakers that control SCN network synchrony and invivo circadian rhythms through intercellular synaptic transmission.
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U2 - 10.1016/j.neuron.2015.02.006
DO - 10.1016/j.neuron.2015.02.006
M3 - Article
C2 - 25741729
AN - SCOPUS:84924257556
SN - 0896-6273
VL - 85
SP - 1086
EP - 1102
JO - Neuron
JF - Neuron
IS - 5
ER -