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Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response.

Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Research Abstract Details 

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  • Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Abstract Text:

    lillian cruz-orengoLillian Cruz-Orengo,johnny d figueroaJohnny D Figueroa,aranza torradoAranza Torrado,anabel puigAnabel Puig,scott r whittemoreScott R Whittemore,jorge d mirandaJorge D Miranda,

    Spinal cord injury (SCI) causes an increase of inhibitory factors that may restrict axonal outgrowth after trauma. During the past decade, the Eph receptors and ephrin ligands have emerged as key repulsive cues known to be involved in neurite outgrowth, synapse formation, and axonal pathfinding during development. Given the non-permissive environment for axonal regeneration after SCI, we questioned whether enhanced-expression of the EphA4 receptor with repulsive activity for axonal outgrowth is potentially responsible for the regenerative failure. To address this possibility, we have examined the expression of EphA4 after SCI in adult rats following a contusion SCI. EphA4 expression studies demonstrated a time-dependent change for EphA4 protein without alterations in beta-actin. EphA4 was downregulated initially and upregulated 7 days after injury. Blockade of EphA4 upregulation with antisense oligonucleotides did not produce an anatomical or physiological response monitored with anterograde tracing studies or transcranial magnetic motor evoked potentials (tcMMEP), respectively. These results demonstrated that upregulation of EphA4 receptors after trauma is not related to axonal regeneration or return of nerve conduction across the injury site.

    Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Publishing Authors By Initials

    l cruz-orengoL Cruz-Orengo,jd figueroaJD Figueroa,a torradoA Torrado,a puigA Puig,sr whittemoreSR Whittemore,jd mirandaJD Miranda,

    For similar diagnosis: diagnostic techniques and procedures: diagnostic techniques, neurological: transcranial magnetic stimulation research abstracts see: diagnosis: diagnostic techniques and procedures: diagnostic techniques, neurological: transcranial magnetic stimulation research

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    Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Neuroscience letters

    VOLUME: 418

    Page Numbers: 49-54

    Journal Abbreviation:

    ISSN: 0304-3940

    DAY: 12

    MONTH: 03

    YEAR: 2007

    Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7600130

    Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Keywords Mesh Terms:

    KEYWORDS: Transcranial Magnetic Stimulation

    MESH TERMS: pathology

    Chemical & Substance for Abstract: Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response. Information

    Substance Name: Receptor, EphA4

    Registry Number: EC 2.7.1.112

    Grant and Affiliation Information for Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response.

    AFFILIATION: Department of Physiology, University of Puerto Rico School of Medicine, San Juan, PR 00936, USA.

    Country: Ireland

    AGENCY: United States NIGMS

    GRANT: S06-GM008224

    ACRONYM: GM

    MEDLINETA: Neurosci Lett

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