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Electrical behaviour of interleukin‐1 beta (IL‐1β) and prostaglandin‐E2 (PGE 2 ) on colonic myenteric neurones
Author(s) -
Kelles A.,
Janssens J.,
Tack J.
Publication year - 2002
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.1365-2982.2002.00336.x
Subject(s) - excitatory postsynaptic potential , tetrodotoxin , postsynaptic potential , myenteric plexus , prostaglandin e2 , hyperpolarization (physics) , depolarization , chemistry , endocrinology , medicine , prostaglandin e , neuroscience , inhibitory postsynaptic potential , biology , receptor , immunohistochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
Abstract Intracellular recordings were used to examine the effects on electrical and synaptic behaviour of interleukin (IL)‐1β and prostaglandin E 2 (PGE 2 ) on myenteric neurones of the guinea‐pig colon. Application of IL‐1β and PGE 2 resulted in a concentration‐dependent slow depolarization with enhanced spike discharge in, respectively, 45% (21/47) and 83% (33/41) of the impaled colonic neurones. Administration of IL‐1β in three neurones (6%) elicited a hyperpolarization. Responses remained during tetrodotoxin application, indicative of a direct effect of both substances on the impaled neurones. The effects of IL‐1β remained in the presence of indomethacine, a prostaglandin synthase inhibitor. Responses were seen in both nitric oxide synthase‐ and choline acetyl transferase‐immunoreactive neurones. IL‐1β evoked a 26% reduction of the fast excitatory postsynaptic potential. These results indicate that the application of IL‐1β and PGE 2 evoke direct excitatory actions on a subset of myenteric neurones. For IL‐1β, direct inhibition and presynaptic inhibition of the fast excitatory postsynaptic potential has also been found. In the distal colon, responses to IL‐1β are not mediated through PGE 2 pathways.