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Interleukin‐1 β selectively increases substance P release and augments the ascending phase of the peristaltic reflex
Author(s) -
Grider J. R.
Publication year - 2003
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1046/j.1350-1925.2003.00445.x
Subject(s) - substance p , vasoactive intestinal peptide , contraction (grammar) , medicine , endocrinology , excitatory postsynaptic potential , reflex , peristalsis , muscle contraction , stimulation , chemistry , muscle relaxation , neuropeptide , biology , inhibitory postsynaptic potential , receptor
Exposure of muscle strips to interleukin (IL)‐1 β stimulates substance P (SP) expression, suggesting a link between IL‐1 β and the increase in SP expression during intestinal inflammation. The present study examined whether the SP expression induced by IL‐1 β is reflected by enhanced SP release and SP‐mediated reflex activity. Exposure of innervated longitudinal colonic muscle strips to IL‐1 β for 8 h increased SP synthesis in, and greater SP release from excitatory motor neurones in response to KCl or electrical field stimulation (EFS), and enhanced longitudinal muscle contraction in response to EFS. IL‐1 Ra and IL‐1 β antibody blocked IL‐1 β ‐induced increase in SP release and muscle contraction. Neither vasoactive intestinal peptide (VIP) nor somatostatin release was increased. The increase in SP release was reflected in enhanced circular muscle contraction in response to stretch. VIP‐mediated descending relaxation of circular muscle was not affected. The selective increase in ascending contraction induced by exposure to IL‐1 β was blocked by IL‐1 Ra or IL‐1 β antibody. We conclude that the selective increase in SP expression induced by IL‐1 β in excitatory motor neurones is reflected by enhanced SP release and longitudinal muscle contraction in response to EFS, and enhanced SP release and circular muscle contraction during the ascending phase of the peristaltic reflex.