Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake

Takashi Matsuda, Takeshi Y. Hiyama, Kenta Kobayashi, Kazuto Kobayashi and Masaharu Noda ()
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Takashi Matsuda: Homeostatic Mechanism Research Unit, Institute of Innovative Research, Tokyo Institute of Technology
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

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-19191-0

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