Journal of dermatological science
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A specialized subpopulation of unmyelinated chemonociceptors and dedicated spinal neurons which are responsible for the itch sensation have been identified recently. Under physiological conditions, painful stimuli such as activation of conventional mechano-heat-sensitive ('polymodal') nociceptors (scratching) inhibit the itch sensation via central mechanisms. ⋯ These mechanisms might well explain the itch in diseases characterized by histamine release like urticaria, and might provide evidence for the role of endogenous opioids as central itch promotors in cholestasis or nephropathy. After the discovery of itch-specific neurons has dramatically improved our understanding of itch mechanisms under experimental conditions, the present task is to correlate these new findings to the clinical situation of itch patients.
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Repeated ultraviolet (UV) irradiations have been shown to induce keratinocyte proliferation with acanthosis, stimulate the cutaneous nerve proliferation, and increase the synthesis of calcitonin gene-related peptide (CGRP). In the current study, we examined the role of CGRP in the UVB-induced proliferation of murine keratinocytes. UVB irradiation increased the number of bromodeoxyuridine (BrdU)-labeled basal keratinocytes and caused acanthosis. ⋯ Intradermal injections of anti-CGRP antibody inhibited the UVB-induced BrdU labeling in basal keratinocytes, but epidermal thickening was not significantly inhibited. These results indicate that CGRP is one of the stimulators to UVB-induced keratinocyte proliferation. On the other hand, expression of substance P, another neuropeptide in the peripheral nerve, was not up-regulated by UVB irradiation.