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Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation.

Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Research Abstract Details 

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  • Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Abstract Text:

    hongru zhaoHongru Zhao,wen zhuWen Zhu,tianhong panTianhong Pan,wenjie xieWenjie Xie,aijun zhangAijun Zhang,william g ondoWilliam G Ondo,weidong leWeidong Le,

    It is suggested that dysfunction of the diencephalospinal dopaminergic (DAergic) pathway may cause restless legs syndrome. We examined the mRNA and protein levels as well as DA receptor subtypes function within the lumbar spinal cord of an RLS animal model. C57BL/6 male mice with or without iron deprivation were lesioned with 6-hydroxydopamine (6-OHDA) in the bilateral A11 nuclei. Locomotor behaviors were observed. DA concentration, mRNA, and protein levels of D1, D2, and D3 receptors in the lumbar spinal cords were analyzed, and the specific binding of D1, D2, and D3 receptors was determined using [(3)H]SCH23390, [(3)H]Spiperone, and [(3)H]PD128907 radioligands respectively. The behavioral tests showed that the locomotor activities were increased significantly in the mice treated with iron-deficiency (ID) diet and 6-OHDA lesions, which were reversed by the D2/D3 agonist ropinirole. DA in the spinal cord was decreased significantly by 6-OHDA lesioning in A11. D2/D3 mRNA and protein levels as well as their binding capacity in the spinal cord were decreased significantly by 6-OHDA lesions. ID with 6-OHDA lesions produced a synergistic greater decrease of D2 binding. Although ID increased D1 mRNA and protein expression in the spinal cord, it did not significantly change D1 receptor binding. The present study suggests that ID and 6-OHDA lesions in A11 nuclei differentially altered the D1, D2, and D3 receptors expression and binding capacity in the lumbar spinal cord of RLS animal model, which was accompanied by changes in locomotor activities.

    Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Publishing Authors By Initials

    h zhaoH Zhao,w zhuW Zhu,t panT Pan,w xieW Xie,a zhangA Zhang,wg ondoWG Ondo,w leW Le,

    For similar nervous system: central nervous system: spinal cord research abstracts see: nervous system: central nervous system: spinal cord research

    PUBMED ID PMID:

    MEDLINE DATE:

    Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Journal Published:

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

    Journal: Journal of neuroscience research

    VOLUME: 85

    Page Numbers: 1065-76

    Journal Abbreviation: J. Neurosci. Res.

    ISSN: 0360-4012

    DAY: 3

    MONTH: Apr

    YEAR: 2007

    Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7600111

    Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Keywords Mesh Terms:

    KEYWORDS: Spinal Cord

    MESH TERMS: physiopathology

    Chemical & Substance for Abstract: Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation. Information

    Substance Name: Iron

    Registry Number: 7439-89-6

    Grant and Affiliation Information for Spinal cord dopamine receptor expression and function in mice with 6-OHDA lesion of the A11 nucleus and dietary iron deprivation.

    AFFILIATION: Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS043567

    ACRONYM: NS

    MEDLINETA: J Neurosci Res

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