{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T06:40:04Z","timestamp":1781851204251,"version":"3.54.5"},"reference-count":64,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2003,12,1]],"date-time":"2003-12-01T00:00:00Z","timestamp":1070236800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2003,12]]},"abstract":"<jats:p>Vagal mechanoreceptors to the guinea\u2010pig oesophagus, recorded extracellularly, <jats:italic>in vitro<\/jats:italic>, fired spontaneously at 3.3 \u00b1 0.2 Hz, (<jats:styled-content><jats:italic>n<\/jats:italic>= 75<\/jats:styled-content>, from 57 animals), and had low thresholds to circumferential stretch. In this study, we have investigated whether mechanotransduction by intraganglionic laminar endings (IGLEs) directly relies on mechano\u2010gated ion channels, or whether it is due to chemical activation by neurotransmitters (glutamate or ATP) released from other cells during mechanical distortion. Rapid distortion of focal transduction sites (IGLEs) evoked action potentials with a latency of &lt; 10 ms. Antagonists to ionotropic (AP5, memantine and 6,7\u2010dinitroquinoxaline\u20102,3\u2010dione (DNQX)) and metabotropic glutamate receptors (<jats:italic>N<\/jats:italic>\u2010phenyl\u20107\u2010(hydroxyimino)cyclopropa[b]chromen\u20101a\u2010carboxamide (PHCCC) and (RS)\u2010a\u2010methyl\u20104\u2010phosphono\u2010phenylglycine (MPPG)) did not affect mechano\u2010transduction. Glutamate, NMDA and the selective mGluR group II and III agonists, (2R, 4R)\u2010APDC and <jats:sc>l<\/jats:sc>\u2010AP4, had no effect on spontaneous or stretch\u2010induced firing. The P2X purinoreceptor agonist, \u03b1,\u03b2\u2010methylene ATP, caused concentration\u2010dependent excitation of vagal mechanoreceptors (EC<jats:sub>50<\/jats:sub>= 22.2 \u00b5<jats:sc>m<\/jats:sc>) which was blocked by the non\u2010selective P2 antagonist PPADS (30 \u00b5<jats:sc>m<\/jats:sc>). On its own, PPADS affected neither stretch\u2010induced firing nor spontaneous firing. Neither Ca<jats:sup>2+<\/jats:sup>\u2010free solution (1 m<jats:sc>m<\/jats:sc> EDTA, 3.6 m<jats:sc>m<\/jats:sc> Mg<jats:sup>2+<\/jats:sup>) solution nor Cd<jats:sup>2+<\/jats:sup> (100 \u00b5<jats:sc>m<\/jats:sc>) blocked stretch\u2010induced firing. Thus chemical transmission is not involved in activation of vagal mechanoreceptors. The blocker of stretch\u2010activated channels, Gd<jats:sup>3+<\/jats:sup> (300 \u00b5<jats:sc>m<\/jats:sc>), did not inhibit stretch\u2010induced firing. However, benzamil (100 \u00b5<jats:sc>m<\/jats:sc>) significantly inhibited spontaneous and distension\u2010evoked firing in a stretch\u2010dependent manner; proportionally greater inhibition was seen with larger stretches. The results suggest that IGLEs of vagal tension receptors directly transduce mechanical stimuli probably via benzamil\u2010sensitive, Gd<jats:sup>3+<\/jats:sup>\u2010insensitive, stretch\u2010activated ion channels, and that chemical transmission is not involved in transduction.<\/jats:p>","DOI":"10.1113\/jphysiol.2003.051862","type":"journal-article","created":{"date-parts":[[2003,9,23]],"date-time":"2003-09-23T01:31:49Z","timestamp":1064280709000},"page":"575-587","source":"Crossref","is-referenced-by-count":127,"title":["Mechanotransduction by intraganglionic laminar endings of vagal tension receptors in the guinea\u2010pig oesophagus"],"prefix":"10.1113","volume":"553","author":[{"given":"Vladimir P.","family":"Zagorodnyuk","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bao Nan","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcello","family":"Costa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon J. 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