Abstract
Our previous studies demonstrate that intrathecal administration of neuropeptide Y (NPY) decreases behavioral and molecular (spinal Fos expression) signs of neuropathic pain. Because these signs are reduced with selective NPY Y1 receptor (Y1) antagonists, we hypothesized that Y1 expression in pain transmission neurons is inversely correlated with allodynia and hyperalgesia. To test this hypothesis, we developed a novel computer-assisted method to quantify Y1 expression in the dorsal horn after transection of the tibial and peroneal nerves, leaving the sural nerve intact (spared nerve injury, SNI, performed under isoflurane anesthesia (5% induction, followed by 2% maintenance)).
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