Propentofylline-induced astrocyte modulation leads to alterations in glial glutamate promoter activation following spinal nerve transection.

摘要: We have previously shown that the atypical methylxanthine, propentofylline, reduces mechanical allodynia after peripheral nerve transection in a rodent model of neuropathy. In present study, we sought to determine whether propentofylline-induced glial modulation alters spinal glutamate transporters, transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) vivo, which may contribute reduced behavioral hypersensitivity injury. order specifically examine expression novel line double transgenic GLT-1-enhanced green fluorescent protein (eGFP)/GLAST-Discosoma Red (DsRed) promoter mice was used. Adult received propentofylline (10 mg/kg) or saline via i.p. injection starting 1 h prior L5-spinal then daily for 12 days. Mice receiving exhibited punctate both eGFP (GLT-1 activation) DsRed (GLAST dorsal horn cord, decreased ipsilateral injury on day 12. Propentofylline administration reinstated activation injured side as evidenced by an equal number puncta horns. As demonstrated previous studies, induced concomitant reversal L5 transection-induced fibrillary acidic (GFAP). The ability alter transporters highlights importance controlling aberrant neuropathic pain suggests one possible mechanism anti-allodynic action this drug.