Abstract
We investigated the P2X4 receptor (P2X4R) expression in the cervical spinal cord, trigeminal ganglion, and infraorbital nerve (ION), after a chronic constriction injury of unilateral ION and a treatment with selective serotonin reuptake inhibitor (SSRI). A recent study has showed that SSRI inhibits P2X4R expression. Injured rats had significantly lower pain thresholds. In injured and slightly injured ION, the P2X4R expression was significantly higher than in the naïve-rat ION. Injured animals with SSRI showed significantly higher pain thresholds than injured animals without the drug. Nonetheless, P2X4R expression in the ipsilateral ION remained high. Immunostaining showed that macrophages are the source of P2X4R. Our results suggest that the expression of P2X4R in our model is modulated not by neuropathic pain, but by slight nerve injury.
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