Changes in [125I]hCGRP binding in rat spinal cord in an experimental model of acute, peripheral inflammation.

[125I]Human calcitonin gene-related peptide ([125I]hCGRP) binding in the dorsal horn of the spinal cord exhibited differential changes among laminae over time in response to unilateral adjuvant-induced inflammation. In laminae I/II, 4 days after induction of inflammation, the binding decreased 36% on the side of the spinal cord ipsilateral to the inflammation, while there was no change on the contralateral side. The decrease ipsilateral to inflammation was due primarily to a decrease in the Bmax of the high affinity binding site for CGRP. In lamina V, the binding increased 18% on both sides of the spinal cord at the same time point. In lamina X, the binding increased 16% on both sides of the spinal cord at 2 days after induction of inflammation and remained increased at 8 days. The increases in [125]hCGRP binding in laminae V and X were primarily due to a decrease in the Kd of the low affinity binding site for CGRP. the accompanying hyperalgesia was first measured at 2 days after induction of inflammation and persisted at 8 days. Because the changes in [125I]hCGRP binding did not parallel the hyperalgesia accompanying the unilateral adjuvant-induced inflammation, we believe that CGRP receptors are not directly involved with the hyperalgesia but may be involved with other plastic changes observed in the spinal cord during unilateral adjuvant-induced inflammation.