Peripheral nerve damage often results in the development of chronic pain states, resistant to classical analgesics. Since vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are up-regulated in dorsal root ganglion cells following peripheral nerve injury, we investigated the expression and influence of VPAC 1 , VPAC 2 and PAC 1 receptors in rat spinal dorsal horn following a chronic constriction injury (CCI). Electrophysiological studies revealed that selective antagonists of VPAC 1 , VPAC 2 and PAC 1 receptors inhibit mustard oil-, but not brush-induced activity of dorsal horn neurones in CCI animals, while cold-induced neuronal activity was attenuated by VPAC 1 and PAC 1 , but not VPAC 2 receptor antagonists. Ionophoresis of selective agonists for the receptor subtypes revealed that the VPAC 2 receptor agonist excited twice as many cells in CCI compared to normal animals, while the number of cells excited by the VPAC 1 receptor agonist decreased and responses to PACAP-38 remained unchanged. In situ hybridisation histochemistry (ISHH) confirmed an increase in the expression of VPAC 2 receptor mRNA within the ipsilateral dorsal horn following neuropathy, while VPAC 1 receptor mRNA was seen to decrease and that for PAC 1 receptors remained unchanged. These data indicate that VIP/PACAP receptors may be important regulatory factors in neuropathic pain states.
Neuropharmacology – Elsevier
Published: Jan 1, 1999
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