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Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain.

Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Research Abstract Details 

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  • Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Abstract Text:

    lillian cruz-orengoLillian Cruz-Orengo,johnny d figueroaJohnny D Figueroa,ixane Ixane ,aranza torradoAranza Torrado,cristina Cristina ,carmen Carmen ,anabel puigAnabel Puig,annabell c segarraAnnabell C Segarra,scott r whittemoreScott R Whittemore,jorge d mirandaJorge D Miranda,

    Spinal cord injury (SCI) is characterized by a total or partial loss of motor and sensory functions due to the inability of neurons to regenerate. This lack of axonal regenerative response has been associated with the induction of inhibitory proteins for regeneration, such as the Eph receptor tyrosine kinases. One member of this family, the EphA4 receptor, coordinates appropriate corticospinal fibers projections during early development and is expressed in spinal commissural interneurons. Its mechanism of action is mediated by repulsive activity after ligand binding, but its role after trauma is unknown. We examined the temporal expression profile of this receptor after spinal cord contusion in adult rats by RT-PCR and immunohistochemistry. SCI induced a biphasic gene expression profile with an initial downregulation at 2 and 4 days post-injury (DPI) followed by a subsequent upregulation. Double labeling studies localized EphA4 immunoreactivity in neurons from the gray matter and astrocytes of the white matter. To test the role of this receptor, we reduced gene upregulation by intrathecal/subdural infusion of EphA4-antisense oligodeoxynucleotide (ODN) and subsequently assessed behavioral outcomes. No locomotor recovery was observed in the rats treated with the EphA4-antisense ODN. Interestingly, reducing EphA4 expression increased mechanical allodynia, as observed by the Von Frey test and decreased exploratory locomotor activity. These results indicate that upregulation of EphA4 receptor after trauma may prevent the development of abnormal pain syndromes and could potentially be exploited as a preventive analgesic mediator to chronic neuropathic pain.

    Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Publishing Authors By Initials

    l cruz-orengoL Cruz-Orengo,jd figueroaJD Figueroa,i I ,a torradoA Torrado,c C ,c C ,a puigA Puig,ac segarraAC Segarra,sr whittemoreSR Whittemore,jd mirandaJD Miranda,

    For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

    PUBMED ID PMID:

    MEDLINE DATE:

    Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Journal Published:

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

    Journal: Experimental neurology

    VOLUME: 202

    Page Numbers: 421-33

    Journal Abbreviation: Exp. Neurol.

    ISSN: 0014-4886

    DAY: 7

    MONTH: 09

    YEAR: 2006

    Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 370712

    Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Keywords Mesh Terms:

    KEYWORDS: Up-Regulation

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain. Information

    Substance Name: Phosphopyruvate Hydratase

    Registry Number: EC 4.2.1.11

    Grant and Affiliation Information for Blocking EphA4 upregulation after spinal cord injury results in enhanced chronic pain.

    AFFILIATION: Department of Physiology, University of Puerto Rico School of Medicine, PO Box 365067 San Juan, PR 00936-5067, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIGMS

    GRANT: S06-GM008224

    ACRONYM: GM

    MEDLINETA: Exp Neurol

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