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Possible Role of P2Y2 Nucleotide Receptor in the Environment Generated After Injury
Author(s) -
Rodriguez Ana E.,
Torrado Aranza,
Figueroa Johnny D.,
Gonzalez Fernando A.,
Miranda Jorge D.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1211
Subject(s) - astrogliosis , ppads , spinal cord injury , receptor , neurite , immunohistochemistry , microbiology and biotechnology , p2 receptor , biology , astrocyte , agonist , neuroscience , medicine , spinal cord , chemistry , immunology , central nervous system , in vitro , biochemistry
Spinal cord injury (SCI) increases inhibitory factors that may restrict neurite outgrowth after trauma. Release of inhibitory molecules and proliferation of reactive astrocytes at the injury site produce a nonpermissive environment for axonal regeneration. The mechanism that triggers astrogliosis is unknown, but the release of nucleotides has been linked to this hypertrophic state. Our goal is to investigate the spatio‐temporal profile of P2Y 2 after SCI. Molecular biology, immunohistochemical (IHC) studies, and behavioral assays were used to evaluate the expression and role of these receptors in rats injured at the T‐10 level using the NYU impactor device. P2Y 2 gene temporal profile using standardized RT‐PCR showed a two‐fold increase after 4–7 days post‐injury (DPI) and returned to basal levels by 14 DPI. IHC studies demonstrated a low level of P2Y 2 receptor in sham samples. After SCI, P2Y 2 receptor expression in GFAP positive cells increased. Intrathecal infusion of suramin and PPADS antagonists resulted in some locomotor recovery. Our results suggest that P2Y 2 receptors may play a role in the establishment of the restrictive environment for axonal regeneration after SCI. Supported by NIH‐MRISP 2R2MH48190‐14, NIH‐SNRP NS39405, MBRS‐SCORE S06‐ GM008224 , MBRS‐RISE GM‐68138, PR‐EPSCOR EPS‐9874782.