{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T14:22:22Z","timestamp":1756995742708},"reference-count":65,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T00:00:00Z","timestamp":1160006400000},"content-version":"vor","delay-in-days":6761,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[1988,4]]},"abstract":"<jats:p><jats:bold>Abstract: <\/jats:bold> The TE671 human medulloblastoma cell line expresses a variety of characteristics of human neurons. Among these characteristics is the expression of membrane\u2010bound high\u2010affinity binding sites for \u03b1\u2010bungarotoxin, which is a potent antagonist of functional nicotinic acetylcholine receptors on these cells. These toxin binding sites represent a class of nicotinic receptor isotypes present in mammalian brain. Treatment of TE671 cells during proliferative growth phase with nicotine or carbamylcholine, but not with muscarine or <jats:italic>d<\/jats:italic>\u2010tubocurarine, induced up to a fivefold increase in the density of radiolabeled toxin binding sites in crude membrane fractions. This effect was blocked by co\u2010incubation with the nicotinic antagonists <jats:italic>d<\/jats:italic>\u2010tubocurarine and decamethonium, but not by mecamylamine or by muscarinic antagonists. Following a 10\u201313 h lag phase upon removal of agonist, recovery of the up\u2010regulated sites to control values occurred within an additional 10\u201320 h. These studies indicate that the expression of functional nicotinic acetylcholine receptors on TE671 cells is subject to regulation by nicotinic agonists. Studies of the murine CNS have consistently indicated nicotine\u2010induced up\u2010regulation of nicotinic acetylcholine receptors, thereby supporting the identification of the toxin binding site on these cells as the functional nicotinic receptor. Although a mechanism for this effect is not apparent, nicotine\u2010induced receptor blockade does not appear to be involved.<\/jats:p>","DOI":"10.1111\/j.1471-4159.1988.tb10604.x","type":"journal-article","created":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T21:12:52Z","timestamp":1160082772000},"page":"1272-1278","source":"Crossref","is-referenced-by-count":19,"title":["Nicotinic Agonists Regulate \u03b1\u2010Bungarotoxin Binding Sites of TE671 Human Medulloblastoma Cells"],"prefix":"10.1111","volume":"50","author":[{"given":"Hal N.","family":"Siegel","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ronald J.","family":"Lukas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,10,5]]},"reference":[{"key":"e_1_2_2_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0149-7634(81)90018-X"},{"key":"e_1_2_2_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-68560-6_2"},{"key":"e_1_2_2_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(82)90195-3"},{"key":"e_1_2_2_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4886(86)90251-7"},{"key":"e_1_2_2_6_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.2.498"},{"key":"e_1_2_2_7_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.24.8374"},{"key":"e_1_2_2_8_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.05-05-01307.1985"},{"key":"e_1_2_2_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0091-3057(86)90518-6"},{"key":"e_1_2_2_10_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.51.070182.002423"},{"key":"e_1_2_2_11_1","first-page":"392","article-title":"[3H]Nicotine binding in rat brain: alteration after chronic acetylcholinesterase inhibition","volume":"226","author":"Costa L. 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