A transient unresponsive state of self-scratching behaviour is induced in mice by skin-scratching stimulation.
When mice were scratched with brushes on their dorsal skins, they began to scratch themselves with their hind paws. Thus, self-scratching behaviour was induced in mice in response to skin-scratching stimulation. If the second skin-scratching stimulation was given within a few days, the induction of the second self-scratching behaviour was significantly suppressed compared with the first one. Thereafter, mice gradually recovered from this unresponsive state within a week. Thus, a transient unresponsive state of self-scratching behaviour is induced by skin-scratching stimulation. Pretreatment with a tachykinin receptor NK-1R antagonist L-703606 or capsaicin significantly suppressed self-scratching behaviour, while pretreatment with a neutral endopeptidase inhibitor phosphoramidon significantly enhanced it. Pretreatment with a calcitonin gene-related peptide (CGRP) receptor antagonist CGRP(8-37) did not affect the following self-scratching behaviour. From these results, it is suggested that substance P (SP) signalling through its receptor NK-1R at least in part mediates the induction of self-scratching behaviour. After skin-scratching stimulation, immunoreactivity of SP both in the peripheral nerve fibres and in the dorsal root ganglion (DRG) neurons was significantly decreased and was well-correlated with suppression of self-scratching behaviour. From these findings, it is suggested that the induction of unresponsive states of self-scratching behaviour may be at least in part caused by the depleted states of SP in peripheral nerve fibres and/or in DRG neurons. The induction of a transient unresponsive state after skin-scratching may possibly happen also in patients with pruritus. Thus, further studies to elucidate the precise mechanisms are required.
Yamaoka
Junichi
J
Department of Dermatology, Nippon Medical School, Sendagi, Bunkyo-ku, Tokyo, Japan. yamaokaj@nms.ac.jp
Kawana
Seiji
S
D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology / Q000502:physiology; D002211:Capsaicin / Q000494:pharmacology; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010446:Peptide Fragments / Q000494:pharmacology; D010812:Physical Stimulation / Q000379:methods*; D011537:Pruritus / Q000503:physiopathology*; D011812:Quinuclidines / Q000494:pharmacology; D012653:Self Stimulation / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D012879:Skin Physiological Phenomena / Q000187:drug effects; D013373:Substance P / Q000502:physiology
D018712:Analgesics, Non-Narcotic; D010446:Peptide Fragments; D011812:Quinuclidines; C058636:calcitonin gene-related peptide (8-37); C076851:L 703606; D013373:Substance P; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin