H1-receptor stimulation induces hyperalgesia through activation of the phospholipase C-PKC pathway
Abstract
The supraspinal cellular events involved in H(1)-mediated hyperalgesia were investigated in a condition of acute thermal pain by means of the mouse hot-plate test. I.c.v. administration of the phospholipase C (PLC) inhibitors U-73122 and neomycin antagonized the hyperalgesia induced by the selective H(1) agonist FMPH. By contrast, U-73343, an analogue of U-73122 used as negative control, was unable to modify the reduction of the pain threshold induced by FMPH. In mice undergoing treatment with LiCl, which impairs phosphatidylinositol synthesis, or treatment with heparin, an IP(3)-receptor antagonist, the hyperalgesia induced by the H(1)-receptor agonist remained unchanged. Similarly, pretreatment with D-myo inositol did not alter the H(1)-induced hypernociceptive response. Neither i.c.v. pretreatment with TMB-8, a blocker of Ca(2+) release from intracellular stores, nor pretreatment with thapsigargin, a depletor of Ca(2+) intracellular stores, prevented the decrease of pain threshold induced by FMPH. On the other hand, i.c.v. pretreatment with the selective protein kinase C (PKC) inhibitors calphostin C and chelerytrine resulted in a dose-dependent prevention of the H(1)-receptor agonist-induced hyperalgesia. The administration...Continue Reading
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Histamine induces microglia activation and dopaminergic neuronal toxicity via H1 receptor activation
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