{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,1]],"date-time":"2026-11-01T16:20:44Z","timestamp":1793550044955,"version":"4.5.0"},"reference-count":80,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2020,7,23]],"date-time":"2020-07-23T00:00:00Z","timestamp":1595462400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2021,5]]},"abstract":"<jats:p>\n                    Neonatal hypoxia-ischemia (nHI) disrupts hippocampal GABAergic development leading to memory deficits in mice. Polysialic-acid neural-cell adhesion molecule (PSA-NCAM) developmentally declines to trigger GABAergic maturation. We hypothesized that nHI changes PSA-NCAM abundance and cellular distribution, impairing GABAergic development, and marking nascent neurodegeneration. Cell degeneration, atrophy, and PSA-NCAM immunoreactivity (IR) were measured in CA1 of nHI-injured C57BL6 mice related to: (i) cellular subtype markers; (ii) GAD65\/67 and synatophysin (SYP), pre-synaptic markers; (iii) phospho-Ser\n                    <jats:sup>396<\/jats:sup>\n                    Tau, cytoskeletal marker; and (iv) GAP43, axonalregeneration marker. PSA-NCAM IR was minimal in CA1 of shams at P11. After nHI, PSA-NCAM IR was increased in injured pyramidal cells (PCs), minimal in parvalbumin (PV)\n                    <jats:sup>+<\/jats:sup>\n                    INs, and absent in glia. PSA-NCAM IR correlated with injury severity and became prominent in perikaryal cytoplasm at P18. GAD65\/67 and SYP IRs only weakly related to PSA-NCAM after nHI. Injured phospho-Ser\n                    <jats:sup>396<\/jats:sup>\n                    Tau\n                    <jats:sup>+<\/jats:sup>\n                    PCs and PV\n                    <jats:sup>+<\/jats:sup>\n                    INs variably co-expressed PSA-NCAM at P40. While PCs with cytoplasmic marginalized PSA-NCAM had increased perisomatic GAP43, those with perikaryal cytoplasmic PSA-NCAM had minimal GAP43. PSA-NCAM increased in serum of nHI-injured mice. Increased PSA-NCAM is likely a generic acute response to nHI brain injury. PSA-NCAM aberrant cellular localization may aggravate neuronal degeneration. The significance of PSA-NCAM as a biomarker of recovery from nHI and nascent neurodegeneration needs further study.\n                  <\/jats:p>","DOI":"10.1177\/0271678x20942707","type":"journal-article","created":{"date-parts":[[2020,7,24]],"date-time":"2020-07-24T01:12:42Z","timestamp":1595553162000},"page":"1039-1057","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":22,"title":["Accumulation of PSA-NCAM marks nascent neurodegeneration in the dorsal hippocampus after neonatal hypoxic-ischemic brain injury in mice"],"prefix":"10.1177","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0788-8028","authenticated-orcid":false,"given":"Raul","family":"Chavez-Valdez","sequence":"first","affiliation":[{"name":"Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, 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