{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T15:24:18Z","timestamp":1783524258958,"version":"3.55.0"},"reference-count":40,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,3,21]],"date-time":"2014-03-21T00:00:00Z","timestamp":1395360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Fetal exposure to alcohol can have multiple deleterious effects, including learning disorders and behavioral and executive functioning abnormalities, collectively termed fetal alcohol spectrum disorders. Neonatal mice lacking both calcium\u2010\/calmodulin\u2010stimulated adenylyl cyclases (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>s) 1 and 8 demonstrate increased vulnerability to ethanol (EtOH)\u2010induced neurotoxicity in the striatum compared with wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) controls. However, the developmental impact on surviving neurons is still unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>WT and <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>1\/8 double knockout (<jats:styled-content style=\"fixed-case\">DKO<\/jats:styled-content>) mice were administered 1 dose of EtOH (2.5\u00a0g\/kg) between postnatal days 5 to 7 (P5\u20137). At P30, brains were removed and processed for Golgi\u2013Cox staining. Medium spiny neurons (<jats:styled-content style=\"fixed-case\">MSN<\/jats:styled-content>s) from the caudate putamen were analyzed for changes in dendritic complexity; number of branches, branch points and terminals, total and average dendritic length; spine density and soma size.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>EtOH significantly reduced the dendritic complexity and soma size in surviving <jats:styled-content style=\"fixed-case\">MSN<\/jats:styled-content>s regardless of genotype without affecting spine density. In the absence of EtOH, genetic deletion of <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>1\/8 reduced the dendritic complexity, number of branch points, spine density, and soma size of <jats:styled-content style=\"fixed-case\">MSN<\/jats:styled-content>s compared with <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These data indicate that neonatal exposure to a single dose of EtOH is sufficient to cause long\u2010term alterations in the dendritic complexity of <jats:styled-content style=\"fixed-case\">MSN<\/jats:styled-content>s and that this outcome is not altered by the functional status of <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>8. Therefore, although deletion of <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>1\/8 demonstrates a role for the ACs in normal morphologic development and EtOH\u2010induced neurodegeneration, loss of <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>1\/8 activity does not exacerbate the effects of EtOH on dendritic morphology or spine density.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12383","type":"journal-article","created":{"date-parts":[[2014,3,21]],"date-time":"2014-03-21T16:23:55Z","timestamp":1395419035000},"page":"1339-1346","source":"Crossref","is-referenced-by-count":15,"title":["Postnatal Ethanol Exposure Simplifies the Dendritic Morphology of Medium Spiny Neurons Independently of Adenylyl Cyclase 1 and 8 Activity in Mice"],"prefix":"10.1111","volume":"38","author":[{"given":"Laura L.","family":"Susick","sequence":"first","affiliation":[{"name":"John D. 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