{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T22:34:59Z","timestamp":1792276499903,"version":"4.4.0"},"reference-count":58,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,2,3]],"date-time":"2005-02-03T00:00:00Z","timestamp":1107388800000},"content-version":"vor","delay-in-days":4204,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[1993,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We know that, once rostral neurulation is completed in the neuroaxis of the chick embryo, the caudal neurocoel becomes occluded and the brain rapidly expands. However, very little is known about the mechanisms maintaining occlusion. Studies had shown that occluded neurocoels reopened in embryos treated with chelators of cations, but the reasons remained unclear and the cations unidentified. To begin defining the role of cations, this study explored the effect of Ca<jats:sup>2+<\/jats:sup>, calmodulin, and cAMP on maintaining the occluded neurocoel. Chick embryos during the natural phase of neurocoel occlusion (stage 12) were cultured in vitro with drugs known to modulate Ca<jats:sup>2+<\/jats:sup> transport, to inhibit calmodulin activity, or to elevate cAMP levels. To test if occlusion is a Ca<jats:sup>2+<\/jats:sup> \u2010dependent process, embryos were treated with verapamil and ionophore A23187. To test if occlusion requires calmodulin, embryos were treated with antipsychotic agents. To test if occlusion is cAMP dependent, embryos were treated with methylisobutylxanthine (MIX), forskolin (FOR), or dibutyl cyclic adenosine (DbC). Following each treatment, occlusion of the neurocoel was tested by injecting dye into the midbrain. All treatments resulted in a predominant number of precocious reopenings of the occluded neurocoels. MIX\u2010treated, naked neural tubes had a fourfold increase in cAMP, whereas FOR\u2010 and DbC\u2010treated neural tubes showed ten\u2010 and 14\u2010fold increases, respectively. The presence of calmodulin in the cells of the neural tube was confirmed by fluorescent tagging and <jats:sup>3<\/jats:sup>H\u2010chlorpromazine labelling. The combined results of this study show that occlusion of the spinal neurocoel depends on exogenous Ca<jats:sup>2+<\/jats:sup>, requires calmodulin, and is cAMP sensitive. \u00a9 1993 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/aja.1001970407","type":"journal-article","created":{"date-parts":[[2005,2,26]],"date-time":"2005-02-26T11:22:54Z","timestamp":1109416974000},"page":"291-306","source":"Crossref","is-referenced-by-count":13,"title":["Second messenger regulation of occlusion of the spinal neurocoel in the chick embryo"],"prefix":"10.1002","volume":"197","author":[{"given":"Mary E.","family":"Desmond","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Duzy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benigno D.","family":"Federici","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,2,3]]},"reference":[{"key":"e_1_2_1_2_1","first-page":"65","volume-title":"Advances Cyclic Nucleotide Research","author":"Appleman M. 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