Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 박현경 | - |
dc.date.accessioned | 2018-03-13T06:39:53Z | - |
dc.date.available | 2018-03-13T06:39:53Z | - |
dc.date.issued | 2013-09 | - |
dc.identifier.citation | Cerebral cortex, Vol.25 No.2 [2015], 482-495 | en_US |
dc.identifier.issn | 1047-3211 | - |
dc.identifier.uri | https://academic.oup.com/cercor/article/25/2/482/303001 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/46076 | - |
dc.description.abstract | The pathophysiology of perinatal brain injury is multifactorial and involves hypoxia-ischemia (HI) and inflammation. N -methyl- d -aspartate receptors (NMDAR) are present on neurons and glia in immature rodents, and NMDAR antagonists are protective in HI models. To enhance clinical translation of rodent data, we examined protein expression of 6 NMDAR subunits in postmortem human brains without injury from 20 postconceptional weeks through adulthood and in cases of periventricular leukomalacia (PVL). We hypothesized that the developing brain is intrinsically vulnerable to excitotoxicity via maturation-specific NMDAR levels and subunit composition. In normal white matter, NR1 and NR2B levels were highest in the preterm period compared with adult. In gray matter, NR2A and NR3A expression were highest near term. NR2A was significantly elevated in PVL white matter, with reduced NR1 and NR3A in gray matter compared with uninjured controls. These data suggest increased NMDAR-mediated vulnerability during early brain development due to an overall upregulation of individual receptors subunits, in particular, the presence of highly calcium permeable NR2B-containing and magnesium-insensitive NR3A NMDARs. These data improve understanding of molecular diversity and heterogeneity of NMDAR subunit expression in human brain development and supports an intrinsic prenatal vulnerability to glutamate-mediated injury; validating NMDAR subunit-specific targeted therapies for PVL. | en_US |
dc.description.sponsorship | This work was supported by the National Institutes of Neurological Disorders and Stroke at the National Institutes of Health (NS 031718 and DP1 OD003347 from the Office of the Director, to F.E.J), the Heart and Stroke Foundation of Canada (to L.L.J), and Alberta Innovates Health Solutions (to L.L.J). This work was also supported by the Boston Children’s Hospital Intellectual and Developmental Disabilities Research Center Cellular Imaging Core (P30 HD18655). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Oxford University Press | en_US |
dc.subject | xcitotoxicity | en_US |
dc.subject | glutamate | en_US |
dc.subject | hypoxia-ischemia | en_US |
dc.subject | N-methyl-d-aspartate | en_US |
dc.subject | periventricular leukomalacia. | en_US |
dc.title | Developmental Expression of N-Methyl-D-Aspartate (NMDA) Receptor Subunits in Human White and Gray Matter: Potential Mechanism of Increased Vulnerability in the Immature Brain | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1093/cercor/bht246 | - |
dc.relation.page | 1-14 | - |
dc.relation.journal | CEREBRAL CORTEX | - |
dc.contributor.googleauthor | Jantzie, Lauren L. | - |
dc.contributor.googleauthor | Talos, Delia M. | - |
dc.contributor.googleauthor | Jackson, Michele C. | - |
dc.contributor.googleauthor | Graham, Dionne A. | - |
dc.contributor.googleauthor | Lechpammer, Mirna | - |
dc.contributor.googleauthor | Folkerth, Rebecca D. | - |
dc.contributor.googleauthor | Volpe, Joseph J. | - |
dc.contributor.googleauthor | Jensen, Frances E. | - |
dc.contributor.googleauthor | Park, Hyun-Kyung | - |
dc.relation.code | 2013009363 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | neopark | - |
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