{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:18:34Z","timestamp":1785406714758,"version":"3.56.0"},"reference-count":101,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T00:00:00Z","timestamp":1781568000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Department of Neonatology, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Germany"},{"name":"\u201cF\u00f6rderverein f\u00fcr fr\u00fchgeborene Kinder an der Charit\u00e9 e.V.\u201d"},{"name":"Sonnenfeld Stiftung, Berlin, Germany"},{"id":[{"id":"https:\/\/ror.org\/04z2zsa77","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Neonatal hyperoxia induces oxidative stress that disrupts neurodevelopmental processes. While dexmedetomidine (DEX) exhibits acute neuroprotective properties, its long-term impact on developmental trajectories during recovery remains incompletely understood. This study examined whether a single neonatal dose of DEX modulates hippocampal neurogenesis following hyperoxia across defined postnatal stages. Six-day-old Wistar rats were exposed to 80% oxygen for 24 h and evaluated at postnatal days (P) 9, 11, and 14 after recovery in room air. Mechanistically, hyperoxia permanently triggered apoptotic cascades, evidenced by sustained transcript upregulation and increased histological apoptosis and cell loss across the cortex and hippocampus, while disrupting the hippocampal progenitor niche, suppressing key differentiation factors (Sox2, Tbr2, Prox1, Calb1) and altering mature NeuN expression. Likewise, markers for autophagy (Atg5\/12, Beclin1), neurotrophins (BDNF, NGF, NT3), and plasticity markers (Nrp1, Sem3a) showed reduced expression. Proactive treatment with DEX (5 \u00b5g\/kg) significantly reversed these detrimental patterns. First, DEX elicited a robust antioxidant response (Nrf2, SOD1, SOD3 induction). Second, DEX effectively suppressed hyperoxia-induced programmed cell death and tissue degeneration up to P14. Crucially, this dual protection sustained the neurogenic niche, safeguarding autophagy processes as well as neurotrophic and neuronal plasticity mediators, while showing excellent safety under normoxia. In conclusion, a single dose of DEX mitigates acute oxygen injury and exhibits beneficial, stage-specific effects within hippocampal neurogenic niches during the postnatal phase, highlighting its potential to preserve neurodevelopmental trajectories.<\/jats:p>","DOI":"10.3390\/cells15121094","type":"journal-article","created":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T09:06:52Z","timestamp":1781600812000},"page":"1094","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dexmedetomidine Preserves Hippocampal Neurogenesis During Recovery from Neonatal Hyperoxia in Rats"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4030-7969","authenticated-orcid":false,"given":"Stefanie","family":"Endesfelder","sequence":"first","affiliation":[{"name":"Department of Neonatology, Charit\u00e9\u2014University Medical Center Berlin, Augustenburger Platz 1, 13353 Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9950-414X","authenticated-orcid":false,"given":"Christoph","family":"B\u00fchrer","sequence":"additional","affiliation":[{"name":"Department of Neonatology, Charit\u00e9\u2014University Medical Center Berlin, Augustenburger Platz 1, 13353 Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Schmitz","sequence":"additional","affiliation":[{"name":"Clinic for Pediatrics and Adolescent Medicine, University Hospital of the Brandenburg Medical School, Fehrbelliner Stra\u00dfe 38, 16816 Neuruppin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,6,16]]},"reference":[{"key":"ref_1","first-page":"Cd004953","article-title":"Sustained versus standard inflations during neonatal resuscitation to prevent mortality and improve respiratory outcomes","volume":"7","author":"Bruschettini","year":"2025","journal-title":"Cochrane Database Syst. 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