The aim of the present study was to investigate the intrathecal (i.t.) action of a selective A1-adenosine receptor agonist, R-phenylisopropyl
adenosine (
R-PIA), on tactile withdrawal thresholds in a rat model of
mononeuropathy produced by sciatic chronic constriction injury (CCI). An additional aim was to examine whether
adenosine receptor activation is involved in the effects of
spinal cord stimulation (SCS), which activates low-threshold fibers and suppresses touch-evoked
pain both in patients and in experimental animals with neuropathy. Animals presenting hindlimb withdrawal to von Frey filaments with a bending force of < 7.5 g on the lesioned side (compared to > or = 35 g in the normal limb), were considered as having tactile
hypersensitivity ("
allodynia').
R-PIA (1-10 nmol i.t.) induced a dose-dependent suppression of the
tactile allodynia without producing impairment of motor function. The effect of
R-PIA (3 nmol i.t.), a clearly submaximal dose, was abolished by concomitant treatment with the selective A1-adenosine receptor antagonist cyclopentylxanthine (10 nmol i.t.). In animals where SCS failed to influence
tactile allodynia, concomitant i.t. administration of
R-PIA (3 nmol) and SCS induced a clear-cut and long-lasting suppression of the
hypersensitivity to tactile stimulation. In conclusion,
adenosine receptor stimulation antagonizes tactile
hypersensitivity in a CCI model of
mononeuropathy and potentiates the action of
spinal cord stimulation.