The role of cholecystokinin in peripheral taste signaling in mice

Ryusuke Yoshida, Misa Shin, Keiko Yasumatsu, Shingo Takai, Mayuko Inoue, Noriatsu Shigemura, Soichi Takiguchi, Seiji Nakamura, Yuzo Ninomiya

研究成果: ジャーナルへの寄稿記事

4 引用 (Scopus)

抄録

Cholecystokinin (CCK) is a gut hormone released from enteroendocrine cells. CCK functions as an anorexigenic factor by acting on CCK receptors expressed on the vagal afferent nerve and hypothalamus with a synergistic interaction between leptin. In the gut, tastants such as amino acids and bitter compounds stimulate CCK release from enteroendocrine cells via activation of taste transduction pathways. CCK is also expressed in taste buds, suggesting potential roles of CCK in taste signaling in the peripheral taste organ. In the present study, we focused on the function of CCK in the initial responses to taste stimulation. CCK was coexpressed with type II taste cell markers such as Ga-gustducin, phospholipase Cß2, and transient receptor potential channel M5. Furthermore, a small subset (~30%) of CCK-expressing taste cells expressed a sweet/umami taste receptor component, taste receptor type 1 member 3, in taste buds. Because type II taste cells are sweet, umami or bitter taste cells, the majority of CCK-expressing taste cells may be bitter taste cells. CCK-A and -B receptors were expressed in both taste cells and gustatory neurons. CCK receptor knockout mice showed reduced neural responses to bitter compounds compared with wild-type mice. Consistently, intravenous injection of CCK-Ar antagonist lorglumide selectively suppressed gustatory nerve responses to bitter compounds. Intravenous injection of CCK-8 transiently increased gustatory nerve activities in a dose-dependent manner whereas administration of CCK-8 did not affect activities of bitter-sensitive taste cells. Collectively, CCK may be a functionally important neurotransmitter or neuromodulator to activate bitter nerve fibers in peripheral taste tissues.

元の言語英語
記事番号866
ジャーナルFrontiers in Physiology
8
発行部数OCT
DOI
出版物ステータス出版済み - 10 31 2017

Fingerprint

Cholecystokinin
Enteroendocrine Cells
Taste Buds
Cholecystokinin Receptors
Intravenous Injections
Neurotransmitter Agents
Cholecystokinin A Receptor
Cholecystokinin B Receptor
Transient Receptor Potential Channels
Phospholipases
Leptin
Nerve Fibers
Knockout Mice

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

これを引用

The role of cholecystokinin in peripheral taste signaling in mice. / Yoshida, Ryusuke; Shin, Misa; Yasumatsu, Keiko; Takai, Shingo; Inoue, Mayuko; Shigemura, Noriatsu; Takiguchi, Soichi; Nakamura, Seiji; Ninomiya, Yuzo.

:: Frontiers in Physiology, 巻 8, 番号 OCT, 866, 31.10.2017.

研究成果: ジャーナルへの寄稿記事

Yoshida, Ryusuke ; Shin, Misa ; Yasumatsu, Keiko ; Takai, Shingo ; Inoue, Mayuko ; Shigemura, Noriatsu ; Takiguchi, Soichi ; Nakamura, Seiji ; Ninomiya, Yuzo. / The role of cholecystokinin in peripheral taste signaling in mice. :: Frontiers in Physiology. 2017 ; 巻 8, 番号 OCT.
@article{906ed115b2ed4997b17c78e3fc17f4a3,
title = "The role of cholecystokinin in peripheral taste signaling in mice",
abstract = "Cholecystokinin (CCK) is a gut hormone released from enteroendocrine cells. CCK functions as an anorexigenic factor by acting on CCK receptors expressed on the vagal afferent nerve and hypothalamus with a synergistic interaction between leptin. In the gut, tastants such as amino acids and bitter compounds stimulate CCK release from enteroendocrine cells via activation of taste transduction pathways. CCK is also expressed in taste buds, suggesting potential roles of CCK in taste signaling in the peripheral taste organ. In the present study, we focused on the function of CCK in the initial responses to taste stimulation. CCK was coexpressed with type II taste cell markers such as Ga-gustducin, phospholipase C{\ss}2, and transient receptor potential channel M5. Furthermore, a small subset (~30{\%}) of CCK-expressing taste cells expressed a sweet/umami taste receptor component, taste receptor type 1 member 3, in taste buds. Because type II taste cells are sweet, umami or bitter taste cells, the majority of CCK-expressing taste cells may be bitter taste cells. CCK-A and -B receptors were expressed in both taste cells and gustatory neurons. CCK receptor knockout mice showed reduced neural responses to bitter compounds compared with wild-type mice. Consistently, intravenous injection of CCK-Ar antagonist lorglumide selectively suppressed gustatory nerve responses to bitter compounds. Intravenous injection of CCK-8 transiently increased gustatory nerve activities in a dose-dependent manner whereas administration of CCK-8 did not affect activities of bitter-sensitive taste cells. Collectively, CCK may be a functionally important neurotransmitter or neuromodulator to activate bitter nerve fibers in peripheral taste tissues.",
author = "Ryusuke Yoshida and Misa Shin and Keiko Yasumatsu and Shingo Takai and Mayuko Inoue and Noriatsu Shigemura and Soichi Takiguchi and Seiji Nakamura and Yuzo Ninomiya",
year = "2017",
month = "10",
day = "31",
doi = "10.3389/fphys.2017.00866",
language = "English",
volume = "8",
journal = "Frontiers in Physiology",
issn = "1664-042X",
publisher = "Frontiers Research Foundation",
number = "OCT",

}

TY - JOUR

T1 - The role of cholecystokinin in peripheral taste signaling in mice

AU - Yoshida, Ryusuke

AU - Shin, Misa

AU - Yasumatsu, Keiko

AU - Takai, Shingo

AU - Inoue, Mayuko

AU - Shigemura, Noriatsu

AU - Takiguchi, Soichi

AU - Nakamura, Seiji

AU - Ninomiya, Yuzo

PY - 2017/10/31

Y1 - 2017/10/31

N2 - Cholecystokinin (CCK) is a gut hormone released from enteroendocrine cells. CCK functions as an anorexigenic factor by acting on CCK receptors expressed on the vagal afferent nerve and hypothalamus with a synergistic interaction between leptin. In the gut, tastants such as amino acids and bitter compounds stimulate CCK release from enteroendocrine cells via activation of taste transduction pathways. CCK is also expressed in taste buds, suggesting potential roles of CCK in taste signaling in the peripheral taste organ. In the present study, we focused on the function of CCK in the initial responses to taste stimulation. CCK was coexpressed with type II taste cell markers such as Ga-gustducin, phospholipase Cß2, and transient receptor potential channel M5. Furthermore, a small subset (~30%) of CCK-expressing taste cells expressed a sweet/umami taste receptor component, taste receptor type 1 member 3, in taste buds. Because type II taste cells are sweet, umami or bitter taste cells, the majority of CCK-expressing taste cells may be bitter taste cells. CCK-A and -B receptors were expressed in both taste cells and gustatory neurons. CCK receptor knockout mice showed reduced neural responses to bitter compounds compared with wild-type mice. Consistently, intravenous injection of CCK-Ar antagonist lorglumide selectively suppressed gustatory nerve responses to bitter compounds. Intravenous injection of CCK-8 transiently increased gustatory nerve activities in a dose-dependent manner whereas administration of CCK-8 did not affect activities of bitter-sensitive taste cells. Collectively, CCK may be a functionally important neurotransmitter or neuromodulator to activate bitter nerve fibers in peripheral taste tissues.

AB - Cholecystokinin (CCK) is a gut hormone released from enteroendocrine cells. CCK functions as an anorexigenic factor by acting on CCK receptors expressed on the vagal afferent nerve and hypothalamus with a synergistic interaction between leptin. In the gut, tastants such as amino acids and bitter compounds stimulate CCK release from enteroendocrine cells via activation of taste transduction pathways. CCK is also expressed in taste buds, suggesting potential roles of CCK in taste signaling in the peripheral taste organ. In the present study, we focused on the function of CCK in the initial responses to taste stimulation. CCK was coexpressed with type II taste cell markers such as Ga-gustducin, phospholipase Cß2, and transient receptor potential channel M5. Furthermore, a small subset (~30%) of CCK-expressing taste cells expressed a sweet/umami taste receptor component, taste receptor type 1 member 3, in taste buds. Because type II taste cells are sweet, umami or bitter taste cells, the majority of CCK-expressing taste cells may be bitter taste cells. CCK-A and -B receptors were expressed in both taste cells and gustatory neurons. CCK receptor knockout mice showed reduced neural responses to bitter compounds compared with wild-type mice. Consistently, intravenous injection of CCK-Ar antagonist lorglumide selectively suppressed gustatory nerve responses to bitter compounds. Intravenous injection of CCK-8 transiently increased gustatory nerve activities in a dose-dependent manner whereas administration of CCK-8 did not affect activities of bitter-sensitive taste cells. Collectively, CCK may be a functionally important neurotransmitter or neuromodulator to activate bitter nerve fibers in peripheral taste tissues.

UR - http://www.scopus.com/inward/record.url?scp=85032702883&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85032702883&partnerID=8YFLogxK

U2 - 10.3389/fphys.2017.00866

DO - 10.3389/fphys.2017.00866

M3 - Article

AN - SCOPUS:85032702883

VL - 8

JO - Frontiers in Physiology

JF - Frontiers in Physiology

SN - 1664-042X

IS - OCT

M1 - 866

ER -