{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:25:56Z","timestamp":1787315156656,"version":"build-2736575974"},"reference-count":39,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":59,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:sec>\n                    <jats:title>Background and purpose:<\/jats:title>\n                    <jats:p>\n                      To characterize the\n                      <jats:italic>in vitro<\/jats:italic>\n                      motor patterns and the neurotransmitters released by enteric motor neurons (EMNs) in the human sigmoid colon.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental approach:<\/jats:title>\n                    <jats:p>Sigmoid circular strips were studied in organ baths. EMNs were stimulated by electrical field stimulation (EFS) and through nicotinic ACh receptors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key results:<\/jats:title>\n                    <jats:p>\n                      Strips developed weak spontaneous rhythmic contractions (3.67\u00b10.49\u2003\n                      <jats:italic>g<\/jats:italic>\n                      , 2.54\u00b10.15\u2003min) unaffected by the neurotoxin tetrodotoxin (TTX; 1\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ). EFS induced strong contractions during (on, 56%) or after electrical stimulus (off, 44%), both abolished by TTX. Nicotine (1\u2013100\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ) inhibited spontaneous contractions. Latency of off\u2010contractions and nicotine responses were reduced by\n                      <jats:italic>N<\/jats:italic>\n                      <jats:sup>G<\/jats:sup>\n                      \u2010nitro\u2010\n                      <jats:sc>L<\/jats:sc>\n                      \u2010arginine (1\u2003m\n                      <jats:sc>M<\/jats:sc>\n                      ) and blocked after further addition of apamin (1\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ) or the P2Y\n                      <jats:sub>1<\/jats:sub>\n                      receptor antagonist MRS 2179 (10\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ) and were unaffected by the P2X antagonist NF279 (10\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ) or \u03b1\u2010chymotrypsin (10\u2003U\u2003mL\n                      <jats:sup>\u22121<\/jats:sup>\n                      ). Amplitude of\n                      <jats:italic>on\u2010<\/jats:italic>\n                      and off\u2010contractions was reduced by atropine (1\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ) and the selective NK\n                      <jats:sub>2<\/jats:sub>\n                      receptor antagonist Bz\u2010Ala\u2010Ala\u2010D\u2010Trp\u2010Phe\u2010D\u2010Pro\u2010Pro\u2010Nle\u2010NH\n                      <jats:sub>2<\/jats:sub>\n                      (1\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ). MRS 2179 reduced the amplitude of EFS on\u2010 and off\u2010contractions without altering direct muscular contractions induced by ACh (1\u2003n\n                      <jats:sc>M<\/jats:sc>\n                      \u20131\u2003m\n                      <jats:sc>M<\/jats:sc>\n                      ) or substance P (1\u2003n\n                      <jats:sc>M<\/jats:sc>\n                      \u201310\u2003\u03bc\n                      <jats:sc>M<\/jats:sc>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and implications:<\/jats:title>\n                    <jats:p>\n                      Latency of EFS\u2010induced off\u2010contractions and inhibition of spontaneous motility by nicotine are caused by stimulation of inhibitory EMNs coreleasing NO and a purine acting at muscular P2Y\n                      <jats:sub>1<\/jats:sub>\n                      receptors through apamin\u2010sensitive K\n                      <jats:sup>+<\/jats:sup>\n                      channels. EFS\u2010induced on\u2010 and off\u2010contractions are caused by stimulation of excitatory EMNs coreleasing ACh and tachykinins acting on muscular muscarinic and NK\n                      <jats:sub>2<\/jats:sub>\n                      receptors. Prejunctional P2Y\n                      <jats:sub>1<\/jats:sub>\n                      receptors might modulate the activity of excitatory EMNs. P2Y\n                      <jats:sub>1<\/jats:sub>\n                      and NK\n                      <jats:sub>2<\/jats:sub>\n                      receptors might be therapeutic targets for colonic motor disorders.\n                    <\/jats:p>\n                    <jats:p>\n                      <jats:italic>British Journal of Pharmacology<\/jats:italic>\n                      (2008)\n                      <jats:bold>155<\/jats:bold>\n                      , 1043\u20131055; doi:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.332\">10.1038\/bjp.2008.332<\/jats:ext-link>\n                      ; published online 1 September 2008\n                    <\/jats:p>\n                  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