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Because the A3 adenosine receptor regulates pain induced by chronic constriction injury or chemotherapy, its stimulation might also attenuate diabetic neuropathy. This study examines the effects of systemic treatment with the A3 adenosine receptor agonist 1\u2010deoxy\u20101\u2010[6\u2010[[(3\u2010iodophenyl)methyl]amino]\u20109<jats:italic>H<\/jats:italic>\u2010purin\u20109\u2010yl]\u2010<jats:italic>N<\/jats:italic>\u2010methyl\u2010\u03b2\u2010d\u2010ribofuranuronamide (IB\u2010MECA) on diabetic neuropathy and explores the putative mechanisms underlying its pharmacological effects. We show that IB\u2010MECA alleviated mechanical hyperalgesia and thermal hypoalgesia in mice 2 weeks but not 4 weeks after streptozocin (STZ) treatment. Furthermore, IB\u2010MECA prevented the reduction in sciatic motor nerve conduction velocity and sensory nerve conduction velocity in diabetic mice 2 weeks but not 4 weeks after STZ treatment. Similarly, IB\u2010MECA inhibited the activation of nuclear factor\u2010\u03baB and decreased the generation of tumor necrosis factor\u2010\u03b1 in the spinal cord of mice 2 weeks but not 4 weeks after STZ treatment. These phenomena were associated with reduction of A3 adenosine receptor expression in the spinal cord after long\u2010term diabetes. 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