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Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding.

Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Research Abstract Details 

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  • Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Abstract Text:

    hongkui zengHongkui Zeng,alexander gragerovAlexander Gragerov,john g hohmannJohn G Hohmann,maria n pavlovaMaria N Pavlova,brian a schimpfBrian A Schimpf,hui xuHui Xu,long-jun wuLong-Jun Wu,hiroki toyodaHiroki Toyoda,ming-gao zhaoMing-Gao Zhao,alex d rohdeAlex D Rohde,galina gragerovaGalina Gragerova,rene onrustRene Onrust,john e bergmannJohn E Bergmann,min zhuoMin Zhuo,george a gaitanarisGeorge A Gaitanaris,

    Neuromedin U (NMU) is a highly conserved neuropeptide with a variety of physiological functions mediated by two receptors, peripheral NMUR1 and central nervous system NMUR2. Here we report the generation and phenotypic characterization of mice deficient in the central nervous system receptor NMUR2. We show that behavioral effects, such as suppression of food intake, enhanced pain response, and excessive grooming induced by intracerebroventricular NMU administration were abolished in the NMUR2 knockout (KO) mice, establishing a causal role for NMUR2 in mediating NMU's central effects on these behaviors. In contrast to the NMU peptide-deficient mice, NMUR2 KO mice appeared normal with regard to stress, anxiety, body weight regulation, and food consumption. However, the NMUR2 KO mice showed reduced pain sensitivity in both the hot plate and formalin tests. Furthermore, facilitated excitatory synaptic transmission in spinal dorsal horn neurons, a mechanism by which NMU stimulates pain, did not occur in NMUR2 KO mice. These results provide significant insights into a functional dissection of the differential contribution of peripherally or centrally acting NMU system. They suggest that NMUR2 plays a more significant role in central pain processing than other brain functions including stress/anxiety and regulation of feeding.

    Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Publishing Authors By Initials

    h zengH Zeng,a gragerovA Gragerov,jg hohmannJG Hohmann,mn pavlovaMN Pavlova,ba schimpfBA Schimpf,h xuH Xu,lj wuLJ Wu,h toyodaH Toyoda,mg zhaoMG Zhao,ad rohdeAD Rohde,g gragerovaG Gragerova,r onrustR Onrust,je bergmannJE Bergmann,m zhuoM Zhuo,ga gaitanarisGA Gaitanaris,

    For similar pathological conditions, signs and symptoms: pathologic processes: stress research abstracts see: pathological conditions, signs and symptoms: pathologic processes: stress research

    PUBMED ID PMID:

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    Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Molecular and cellular biology

    VOLUME: 26

    Page Numbers: 9352-63

    Journal Abbreviation: Mol. Cell. Biol.

    ISSN: 0270-7306

    DAY: 9

    MONTH: 10

    YEAR: 2006

    Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8109087

    Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Keywords Mesh Terms:

    KEYWORDS: Stress

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding. Information

    Substance Name: neuromedin U receptor

    Registry Number: 0

    Grant and Affiliation Information for Neuromedin U receptor 2-deficient mice display differential responses in sensory perception, stress, and feeding.

    AFFILIATION: Nura, Inc., Seattle, WA 98104, USA. hzeng@omeros.com

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIMH

    GRANT: MH070241

    ACRONYM: MH

    MEDLINETA: Mol Cell Biol

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