Premium
Role of gastrin‐releasing peptide and neuromedin B receptors in the neurotransmission of itch in the spinal cord of mice
Author(s) -
Sukhtankar Devki,
Ko Meichuan
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1176.6
Subject(s) - scratching , bombesin , gastrin releasing peptide , chemistry , spinal cord , receptor , endocrinology , medicine , neuropeptide , antagonist , neurotransmission , pharmacology , neuroscience , biology , physics , acoustics
Bombesin is a pruritogen which, when centrally administered, causes intense scratching across several animal species. Bombesin has high affinity for receptors of gastrin‐releasing peptide (GRPr) and neuromedin B (NMBr). Studies from GRPr mutant mice and ablated GRPr neurons propose that spinal GRPr are central mediators regulating itch. However, at supraspinal sites, GRPr and NMBr independently mediate scratching behaviors in rats. It is not known to what degree spinal GRPr selectively or generally regulate scratching behavior in mice. To determine if spinal GRPr mediate scratching induced by bombesin‐like ligands, mice were injected with bombesin (0.01–0.3nmol), GRP (0.01–0.3nmol) or NMB (0.1–1nmol) intrathecally by lumbar puncture and were observed for one hour. Bombesin induced most profound scratching that lasted an entire hour while NMB elicited least scratching for a short duration of 15 min. Pretreatment (10 min) with intrathecal injection of a GRPr antagonist RC‐3095 (0.03–0.1 nmol) produced rightward parallel shift in the dose response curve of GRP‐induced scratching but did not diminish bombesin‐or NMB‐induced scratching. Hence, these pharmacological data indicate that the spinal GRPr is only one of the central itch mediators and that there are additional non‐GRPr in the mouse spinal cord regulating neurotransmission of itch (Supported by NIAMS‐R01‐AR059193).