Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons

Shahid Mohammad; Tomoya Ozaki; Kouhei Takeuchi; Katsuya Unno; Kurumi Yamoto; Eri Morioka; Soichi Takiguchi; Masayuki Ikeda

doi:10.1074/jbc.M112.416214

Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons

Shahid Mohammad, Tomoya Ozaki, Kouhei Takeuchi, Katsuya Unno, Kurumi Yamoto, Eri Morioka, Soichi Takiguchi, Masayuki Ikeda^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

Background: Cholecystokinin (CCK)-1 receptor ligands control satiety. Normal intake behaviors in the receptor gene knock-out mice, however, raise questions for CCK-mediated satiety control. Results: CCK-1 receptor gene knock-out facilitated CCK-2 receptor signaling in the posterior paraventricular nucleus and switched receptor subtypes responsible for satiety control. Conclusion: Synergic interaction between CCK-1 and -2 receptors guarantees regular intakes. Significance: Compensatory receptor functions shed light on CCK-mediated satiety controlling mechanism.

Original language	English
Pages (from-to)	39391-39401
Number of pages	11
Journal	Journal of Biological Chemistry
Volume	287
Issue number	47
DOIs	https://doi.org/10.1074/jbc.M112.416214
State	Published - 2012/11/16

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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title = "Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons",

abstract = "Background: Cholecystokinin (CCK)-1 receptor ligands control satiety. Normal intake behaviors in the receptor gene knock-out mice, however, raise questions for CCK-mediated satiety control. Results: CCK-1 receptor gene knock-out facilitated CCK-2 receptor signaling in the posterior paraventricular nucleus and switched receptor subtypes responsible for satiety control. Conclusion: Synergic interaction between CCK-1 and -2 receptors guarantees regular intakes. Significance: Compensatory receptor functions shed light on CCK-mediated satiety controlling mechanism.",

author = "Shahid Mohammad and Tomoya Ozaki and Kouhei Takeuchi and Katsuya Unno and Kurumi Yamoto and Eri Morioka and Soichi Takiguchi and Masayuki Ikeda",

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doi = "10.1074/jbc.M112.416214",

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TY - JOUR

T1 - Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons

AU - Mohammad, Shahid

AU - Ozaki, Tomoya

AU - Takeuchi, Kouhei

AU - Unno, Katsuya

AU - Yamoto, Kurumi

AU - Morioka, Eri

AU - Takiguchi, Soichi

AU - Ikeda, Masayuki

PY - 2012/11/16

Y1 - 2012/11/16

N2 - Background: Cholecystokinin (CCK)-1 receptor ligands control satiety. Normal intake behaviors in the receptor gene knock-out mice, however, raise questions for CCK-mediated satiety control. Results: CCK-1 receptor gene knock-out facilitated CCK-2 receptor signaling in the posterior paraventricular nucleus and switched receptor subtypes responsible for satiety control. Conclusion: Synergic interaction between CCK-1 and -2 receptors guarantees regular intakes. Significance: Compensatory receptor functions shed light on CCK-mediated satiety controlling mechanism.

AB - Background: Cholecystokinin (CCK)-1 receptor ligands control satiety. Normal intake behaviors in the receptor gene knock-out mice, however, raise questions for CCK-mediated satiety control. Results: CCK-1 receptor gene knock-out facilitated CCK-2 receptor signaling in the posterior paraventricular nucleus and switched receptor subtypes responsible for satiety control. Conclusion: Synergic interaction between CCK-1 and -2 receptors guarantees regular intakes. Significance: Compensatory receptor functions shed light on CCK-mediated satiety controlling mechanism.

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SN - 0021-9258

VL - 287

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JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 47

ER -

Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons

Abstract

ASJC Scopus subject areas

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