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R‐type Ca 2+ Channels Contribute to Neural Control of Murine Colonic Motility
Author(s) -
Skylis Laura,
Galligan James,
RodriguezTapia Eileen
Publication year - 2015
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.29.1_supplement.1002.20
Subject(s) - tetrodotoxin , motility , neurotransmitter , in vivo , chemistry , endocrinology , interstitial cell of cajal , medicine , in vitro , contraction (grammar) , conotoxin , migrating motor complex , biophysics , biology , smooth muscle , biochemistry , central nervous system , microbiology and biotechnology , peptide
Background The enteric nervous system controls gastrointestinal motility. Multiple subtypes of voltage‐gated Ca 2+ channels contribute to neurotransmitter release from enteric neurons. Objective We tested the hypothesis that R‐type Ca 2+ channels contribute to enteric neurotransmitter release in the mouse colon. Methods Studies were done in vivo and in vitro using wild type (WT) and a1E Ca 2+ channel (R‐type) knockout (KO) mice. Fecal output was measured in vivo . The colonic migrating motor complex (CMMC) was measured in vitro . We used NiCl 2 (50 mM) to block R‐type Ca 2+ channels , Ω‐conotoxin (CTX, 0.1 mM) to block N‐type Ca 2+ channels and tetrodotoxin (TTX, Na + channel blocker, 0.3 mM) on CMMCs. Results There was no significant difference in fecal output between a1E KO and WT mice. There was no difference in the frequency, propagation speed or amplitude of CMMC contractions between colons from WT and a1E KO mice. NiCl 2 slightly decreased contraction amplitude in colons from a1E KO and WT mice. CTX and TTX completely blocked neurogenic contractions and disrupted the CMMC pattern, leaving only spontaneous myogenic contractions behind. Conclusion These results suggest that either R‐type Ca 2+ channels have a minor role in controlling colonic motility, or that there is compensatory upregulation of other Ca 2+ types in the constitutive a1E KO mice. * Supported by: R01DK094932