{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:56:13Z","timestamp":1772160973667,"version":"3.50.1"},"reference-count":115,"publisher":"Wiley","issue":"24","license":[{"start":{"date-parts":[[2021,11,26]],"date-time":"2021-11-26T00:00:00Z","timestamp":1637884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2021,12]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Intentional ingestion of agricultural organophosphorus insecticides is a significant public health issue in rural Asia, causing thousands of deaths annually. Some survivors develop a severe, acute or delayed myasthenic syndrome. In animal models, similar myasthenia has been associated with increasing plasma concentration of one insecticide solvent metabolite, cyclohexanol. We investigated possible mechanisms using voltage and current recordings from mouse neuromuscular junctions (NMJs) and transfected human cell lines. Cyclohexanol (10\u201325\u00a0mM) reduced endplate potential (EPP) amplitudes by 10\u201340% and enhanced depression during repetitive (2\u201320\u00a0Hz) stimulation by up to 60%. EPP decay was prolonged more than twofold. Miniature EPPs were attenuated by more than 50%. Cyclohexanol inhibited whole\u2010cell currents recorded from CN21 cells expressing human postjunctional acetylcholine receptors (hnAChR) with an IC\n                      <jats:sub>50<\/jats:sub>\n                      of 3.74\u00a0mM. Cyclohexanol (10\u201320\u00a0mM) also caused prolonged episodes of reduced\u2010current, multi\u2010channel bursting in outside\u2010out patch recordings from hnAChRs expressed in transfected HEK293T cells, reducing charge transfer by more than 50%. Molecular modelling indicated cyclohexanol binding (\u22126\u00a0kcal\/mol) to a previously identified alcohol binding site on nicotinic AChR \u03b1\u2010subunits. Cyclohexanol also increased quantal content of evoked transmitter release by \u223c50%. In perineurial recordings, cyclohexanol selectively inhibited presynaptic K\n                      <jats:sup>+<\/jats:sup>\n                      currents. Modelling indicated cyclohexanol binding (\u22123.8\u00a0kcal\/mol) to voltage\u2010sensitive K\n                      <jats:sup>+<\/jats:sup>\n                      channels at the same site as tetraethylammonium (TEA). TEA (10\u00a0mM) blocked K\n                      <jats:sup>+<\/jats:sup>\n                      channels more effectively than cyclohexanol but EPPs were more prolonged in 20\u00a0mM cyclohexanol. The results explain the pattern of neuromuscular dysfunction following ingestion of organophosphorus insecticides containing cyclohexanol precursors and suggest that cyclohexanol may facilitate investigation of mechanisms regulating synaptic strength at NMJs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Intentional ingestion of agricultural organophosphorus insecticides is a significant public health issue in rural Asia, causing thousands of deaths annually. Survivors may develop a severe myasthenic syndrome or paralysis, associated with increased plasma levels of cyclohexanol, an insecticide solvent metabolite.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Analysis of synaptic transmission at neuromuscular junctions in isolated mouse skeletal muscle, using isometric tension recording and microelectrode recording of endplate voltages and currents, showed that cyclohexanol reduced postsynaptic sensitivity to acetylcholine neurotransmitter (reduced quantal size) while simultaneously enhancing evoked transmitter release (increased quantal content).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Patch recording from transfected cell lines, together with molecular modelling, indicated that cyclohexanol causes selective, allosteric antagonism of postsynaptic nicotinic acetylcholine receptors and block of presynaptic K\n                            <jats:sup>+<\/jats:sup>\n                            \u2010channel function.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The data provide insight into the cellular and molecular mechanisms of neuromuscular weakness following intentional ingestion of agricultural organophosphorus insecticides. Our findings also extend understanding of the effects of alcohols on synaptic transmission and homeostatic synaptic function.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp281921","type":"journal-article","created":{"date-parts":[[2021,11,8]],"date-time":"2021-11-08T16:40:25Z","timestamp":1636389625000},"page":"5417-5449","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Antagonistic postsynaptic and presynaptic actions of cyclohexanol on neuromuscular synaptic transmission and function"],"prefix":"10.1113","volume":"599","author":[{"given":"Kosala N.","family":"Dissanayake","sequence":"first","affiliation":[{"name":"Centre for Discovery Brain Sciences University of Edinburgh Edinburgh UK"},{"name":"Pharmacology, Toxicology and Therapeutics Centre for Cardiovascular Science Queen's Medical Research Institute University of Edinburgh Edinburgh UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Filip","family":"Margetiny","sequence":"additional","affiliation":[{"name":"Centre for Discovery Brain Sciences University of Edinburgh Edinburgh UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charlotte L.","family":"Whitmore","sequence":"additional","affiliation":[{"name":"Toxicology, Trauma and Medicine Group Dstl, Porton Down Salisbury UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert C.\u2010C.","family":"Chou","sequence":"additional","affiliation":[{"name":"Centre for Discovery Brain Sciences University of Edinburgh Edinburgh UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cornelia","family":"Roesl","sequence":"additional","affiliation":[{"name":"Centre for Discovery Brain Sciences University of Edinburgh Edinburgh UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vishwendra","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Physiology and Neuroscience, Rutgers State University of New Jersey Newark NJ USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3225-6372","authenticated-orcid":false,"given":"Joseph J.","family":"McArdle","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Physiology and Neuroscience, Rutgers State University of New Jersey Newark NJ USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7893-1348","authenticated-orcid":false,"given":"Richard","family":"Webster","sequence":"additional","affiliation":[{"name":"Weatherall Institute for Molecular Medicine Radcliffe Infirmary Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9395-7132","authenticated-orcid":false,"given":"David","family":"Beeson","sequence":"additional","affiliation":[{"name":"Weatherall Institute for Molecular Medicine Radcliffe Infirmary Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5670-7134","authenticated-orcid":false,"given":"John E.H.","family":"Tattersall","sequence":"additional","affiliation":[{"name":"Toxicology, Trauma and Medicine Group Dstl, Porton Down Salisbury UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4957-6049","authenticated-orcid":false,"given":"David J. 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