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However, how activity\u2010dependent<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>expression affects specific cholinergic gene expression remains unclear. This study addressed this question by determining<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>levels of 22 acetylcholine receptor subunits, the choline transporter (<jats:styled-content style=\"fixed-case\">CHT<\/jats:styled-content>), and the choline acetyltransferase (Ch<jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>) in mice deficient in activity\u2010dependent<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>via promoter<jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content>(<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>) and control wild\u2010type mice. Quantitative<jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>revealed significant reductions in nicotinic acetylcholine receptor alpha 5 (<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>5) in the frontal cortex and hippocampus and M5 muscarinic acetylcholine receptor (<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>5) in the hippocampus, but significant increases in M2 muscarinic acetylcholine receptor (<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>2) in the frontal cortex of<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>mice compared to wild\u2010type mice. Three\u2010week treatments with fluoxetine, phenelzine, duloxetine, imipramine, or an enriched environment treatment (<jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>) did not affect the altered expression of these genes except that<jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>increased<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>5 levels only in<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>frontal cortex.<jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>also increased levels of<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>7,<jats:styled-content style=\"fixed-case\">CHT<\/jats:styled-content>, and Ch<jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>, again only in the<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>frontal cortex. The imipramine treatment was most prominent among the four antidepressants; it up\u2010regulated hippocampal<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>2 and frontal cortex<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>5 in both genotypes, and frontal cortex<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>7 only in<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>mice. To the best of our knowledge, this is the first evidence that<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>deficiency disturbs expression of<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>5,<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>2, and<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>5. Our results suggest that promoter<jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>deficiency \u2013 which occurs under chronic stress \u2013 causes cholinergic dysfunctions via these receptors.<jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>is effective on<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>5, while its compensatory induction of other cholinergic genes or drugs targeting<jats:styled-content style=\"fixed-case\">CHRNA<\/jats:styled-content>5,<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>2, and<jats:styled-content style=\"fixed-case\">CHRM<\/jats:styled-content>5 may become an alternative strategy to reverse these<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>\u2010linked cholinergic dysfunctions.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p><jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc14129-fig-0005-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.14129","type":"journal-article","created":{"date-parts":[[2017,7,19]],"date-time":"2017-07-19T15:36:03Z","timestamp":1500478563000},"page":"49-64","source":"Crossref","is-referenced-by-count":15,"title":["Promoter<scp>IV<\/scp>\u2010<scp>BDNF<\/scp>deficiency disturbs cholinergic gene expression of<scp>CHRNA<\/scp>5,<scp>CHRM<\/scp>2, and<scp>CHRM<\/scp>5: effects of drug and environmental treatments"],"prefix":"10.1111","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6509-216X","authenticated-orcid":false,"given":"Kazuko","family":"Sakata","sequence":"first","affiliation":[{"name":"Department of Pharmacology University of Tennessee Health Science Center Memphis TN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abigail E.","family":"Overacre","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of Tennessee Health Science Center Memphis TN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2017,8,16]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21139"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(90)90166-D"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2007.06.033"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2001.00234.x"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2258-10.2010"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/tp.2014.23"},{"key":"e_1_2_7_8_1","first-page":"431","volume-title":"Drugs and the treatment of psychiatric disorders","author":"Baldessarini R. 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