{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T09:33:36Z","timestamp":1791192816403,"version":"4.1.0"},"reference-count":54,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2013,2,13]],"date-time":"2013-02-13T00:00:00Z","timestamp":1360713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Brain\u2010derived neurotrophic factor (<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>) is implicated in the pathophysiology of major depression; mice lacking <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> expression through promoter <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content>) exhibit a depression\u2010like phenotype. We tested our hypothesis that deficits caused by promoter <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content> deficiency (depression\u2010like behavior, decreased levels of <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>, and neurogenesis in the hippocampus) could be rescued by a 3\u2010week treatment with different types of antidepressants: fluoxetine, phenelzine, duloxetine, or imipramine. Each antidepressant reduced immobility time in the tail suspension test without affecting locomotor activity in the open field test in both <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content> and control wild type mice, except that phenelzine increased locomotor activity in wild type mice and anxiety\u2010like behavior in <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content> mice. The antidepressant treatments were insufficient to reverse decreased <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> levels caused by promoter <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content> deficiency. No antidepressant treatment increased the hippocampal progenitors of either genotype, whereas phenelzine decreased the surviving progenitors in both genotypes. The antidepressant treatments differently affected the dendritic extension of hippocampal immature neurons: fluoxetine and imipramine increased extension in both genotypes, duloxetine increased it only in <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KIV<\/jats:styled-content> mice, and phenelzine decreased it only in wild type mice. Interestingly, a saline\u2010only injection increased neurogenesis and dendrite extensions in both genotypes. Our results indicate that the behavioral effects in the tail suspension test by antidepressants do not require promoter <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content>\u2010driven <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> expression and occur without a detectable increase in hippocampal <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> levels and neurogenesis but may involve increased dendritic reorganisation of immature neurons. In conclusion, the antidepressant treatment demonstrated limited efficacy; it partially reversed the defective phenotypes caused by promoter <jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content> deficiency but not hippocampal <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> levels.<\/jats:p>","DOI":"10.1111\/ejn.12148","type":"journal-article","created":{"date-parts":[[2013,2,14]],"date-time":"2013-02-14T00:56:40Z","timestamp":1360803400000},"page":"1863-1874","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Effects of antidepressant treatment on mice lacking brain\u2010derived neurotrophic factor expression through promoter <scp>IV<\/scp>"],"prefix":"10.1111","volume":"37","author":[{"given":"Kazuko","family":"Sakata","sequence":"first","affiliation":[{"name":"Department of Pharmacology\/Psychiatry College of Medicine University of Tennessee Health Science Center 874 Union 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