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Ethanol (EtOH) exposure during this period is results in a loss of tissue volume and associated neurobehavioral deficits. However, mechanisms that link EtOH exposure to teratology in these regions are not well understood. We therefore analyzed transcriptomic adaptations to EtOH exposure to identify mechanistic linkages.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Hippocampi and cerebella were microdissected at postnatal day (P)10, from control C57BL\/6J mouse pups, and pups treated with 4\u00a0g\/kg of EtOH from P4 to P9. RNA was isolated and RNA\u2010seq analysis was performed. We compared gene expression in EtOH\u2010 and vehicle\u2010treated control neonates and performed biological pathway\u2010overrepresentation analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>While EtOH exposure resulted in the general induction of genes associated with the S\u2010phase of mitosis in both cerebellum and hippocampus, overall there was little overlap in differentially regulated genes and associated biological pathways between these regions. In cerebellum, EtOH additionally induced gene expression associated with the G2\/M\u2010phases of the cell cycle and sonic hedgehog signaling, while in hippocampus, EtOH\u2010induced the pathways for ribosome biogenesis and protein translation. Moreover, EtOH inhibited the transcriptomic identities associated with inhibitory interneuron subpopulations in the hippocampus, while in the cerebellum there was a more pronounced inhibition of transcripts across multiple oligodendrocyte maturation stages.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These data indicate that during the delayed neurogenic period, EtOH may stimulate the cell cycle, but it otherwise results in widely divergent molecular effects in the hippocampus and cerebellum. Moreover, these data provide evidence for region\u2010 and cell\u2010type\u2010specific vulnerability, which may contribute to the pathogenic effects of developmental EtOH exposure.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.14633","type":"journal-article","created":{"date-parts":[[2021,6,1]],"date-time":"2021-06-01T04:17:14Z","timestamp":1622521034000},"page":"1408-1423","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period"],"prefix":"10.1111","volume":"45","author":[{"given":"Marisa R.","family":"Pinson","sequence":"first","affiliation":[{"name":"Department of Neuroscience and Experimental Therapeutics Texas A&amp;M University Health Science Center  Bryan TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kalee N.","family":"Holloway","sequence":"additional","affiliation":[{"name":"Department of Neurobiology and Developmental Sciences University of Arkansas for Medical Sciences  Little Rock AR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James C.","family":"Douglas","sequence":"additional","affiliation":[{"name":"Department of Neurobiology and Developmental Sciences University of Arkansas for Medical Sciences  Little Rock AR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cynthia J. 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