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This study investigated the effects of gabapentin on spinal α2/δ-1 subunit of voltage-gated calcium channels (VGCCs), fractalkine, CX3CR1 expression levels and glial activation, as well as thermal hyperalgesia evoked by monoarthritis (MA).MA produced a robust upregulation of VGCCs α2/δ-1 subunit, fractaline, CX3CR1 expression levels, and activation of microglia and astrocytes in the spinal cord, which was associated with the development of thermal hyperalgesia.Immunofluorescence showed that α2/δδ-1 subunit of VGCCs, a proposed action target of gabapentin, was wildly distributed in primary afferent fibers terminals and dorsal horn neurons.Fractalkine, a potential trigger to activate microglia, colocalized with α2/δ-1 subunit of VGCCs in superficial spinal cord, whereas its receptor CX3CR1 was mainly expressed in spinal mieroglia.Intraperitoneal (i.p.) gabapentin significantly downregulated spinal α2/δ-1 subunit of VGCCs and fractalkine levels, suppressed microglial activation and blocked the development of thermal hyperalgesia in MA rats.These data suggest that gabapentin may diminish fractalkine release in the spinal cord via modulating α2/δ-1 subunit of VGCCs, thereby leading to the reduction in spinal glial activation and thermal hyperalgesia.