Author
Listed:
- Takashi Matsuda
(Homeostatic Mechanism Research Unit, Institute of Innovative Research, Tokyo Institute of Technology
Division of Molecular Neurobiology, National Institute for Basic Biology)
- Takeshi Y. Hiyama
(Division of Molecular Neurobiology, National Institute for Basic Biology)
- Kenta Kobayashi
(Section of Viral Vector Development, National Institute for Physiological Sciences)
- Kazuto Kobayashi
(Fukushima Medical University School of Medicine)
- Masaharu Noda
(Homeostatic Mechanism Research Unit, Institute of Innovative Research, Tokyo Institute of Technology
Division of Molecular Neurobiology, National Institute for Basic Biology)
Abstract
The control of water-intake behavior is critical for life because an excessive water intake induces pathological conditions, such as hyponatremia or water intoxication. However, the brain mechanisms controlling water intake currently remain unclear. We previously reported that thirst-driving neurons (water neurons) in the subfornical organ (SFO) are cholecystokinin (CCK)-dependently suppressed by GABAergic interneurons under Na-depleted conditions. We herein show that CCK-producing excitatory neurons in the SFO stimulate the activity of GABAergic interneurons via CCK-B receptors. Fluorescence-microscopic Ca2+ imaging demonstrates two distinct subpopulations in CCK-positive neurons in the SFO, which are persistently activated under hyponatremic conditions or transiently activated in response to water drinking, respectively. Optical and chemogenetic silencings of the respective types of CCK-positive neurons both significantly increase water intake under water-repleted conditions. The present study thus reveals CCK-mediated neural mechanisms in the central nervous system for the control of water-intake behaviors.
Suggested Citation
Takashi Matsuda & Takeshi Y. Hiyama & Kenta Kobayashi & Kazuto Kobayashi & Masaharu Noda, 2020.
"Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake,"
Nature Communications, Nature, vol. 11(1), pages 1-15, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19191-0
DOI: 10.1038/s41467-020-19191-0
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