Abstract
The neurokinin receptors NK1 and NK3 are involved in processing nociceptive information in the spinal dorsal horn and in central changes following persistent peripheral injury. However, little is known about functional changes in these receptor systems, particularly the NK3 receptor. We have performed intracellular recordings from spinal dorsal horn neurons in vitro, using spinal cords obtained both from control rats and from those with a peripheral inflammation induced by carrageenan. Application of the NK1 receptor agonist, [Sar 9, Met(O 2) 11]Substance P and the NK3 receptor agonist, Senktide, produced slow, long lasting depolarizations. The Senktide- but not [Sar 9, Met(O 2) 11]Substance P-induced depolarizations were significantly smaller in carrageenan-treated rats. These data indicate an altered role for the NK3 receptor in the spinal dorsal horn following acute peripheral inflammation.
Published Version
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