{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T16:57:45Z","timestamp":1773939465538,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2012,10,29]],"date-time":"2012-10-29T00:00:00Z","timestamp":1351468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2012,11]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Decreased baroreflex sensitivity is associated with poor outcome in many cardiovascular diseases including stroke, but the molecular mechanism underlying this relationship is unclear. This work was designed to test the hypothesis that acetylcholine (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h) and \u03b17 nicotinic <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h receptor (\u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>) mediate the protection of arterial baroreflex against stroke.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Sinoaortic denervation (<jats:styled-content style=\"fixed-case\">SAD<\/jats:styled-content>) was used to impair the function of arterial baroreflex, and anticholinesterase agents were used to activate the cholinergic system and increase endogenous <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h. Middle cerebral artery occlusion (<jats:styled-content style=\"fixed-case\">MCAO<\/jats:styled-content>) was performed in the \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> knockout (<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>) mice and <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>prague\u2013<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>awley rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found decreased expression of vesicular <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h transporter (<jats:styled-content style=\"fixed-case\">VAC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>) and \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> in rat brain after <jats:styled-content style=\"fixed-case\">SAD<\/jats:styled-content>. In rats subjected to <jats:styled-content style=\"fixed-case\">MCAO<\/jats:styled-content>, neostigmine significantly reduced the infarct size. The protective effects of neostigmine were abolished by selective n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> antagonist vecuronium but not by m<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> antagonist anisodamine. In addition, the effect of neostigmine disappeared in \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R KO<\/jats:styled-content> mice. In cultured neurons, <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h inhibited cell death induced by <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content><jats:sub>2<\/jats:sub><jats:styled-content style=\"fixed-case\">O<\/jats:styled-content><jats:sub>2<\/jats:sub>. In cultured microglial cells, <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h decreased the release of proinflammatory cytokines induced by lipopolysaccharide. These <jats:italic>in vitro<\/jats:italic> effects were blocked by selective \u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> antagonists.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Taken together, these findings indicate that the <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h\u2010\u03b17n<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content> involved in the protective effects of arterial baroreflex against ischemic stroke.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12011","type":"journal-article","created":{"date-parts":[[2012,10,29]],"date-time":"2012-10-29T18:58:22Z","timestamp":1351537102000},"page":"918-926","source":"Crossref","is-referenced-by-count":33,"title":["Involvement of Acetylcholine\u2010\u03b17n<scp>AC<\/scp>h<scp>R<\/scp> in the Protective 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