Developmental regulation of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. II. Human cerebral white matter and cortex

This report is the second of a two‐part evaluation of developmental differences in α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐propionic acid receptor (AMPAR) subunit expression in cell populations within white matter and cortex. In part I, we reported that, in rat, developmental expression of Ca2+‐perme...

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Published inJournal of comparative neurology (1911) Vol. 497; no. 1; pp. 61 - 77
Main Authors Talos, Delia M., Follett, Pamela L., Folkerth, Rebecca D., Fishman, Rachel E., Trachtenberg, Felicia L., Volpe, Joseph J., Jensen, Frances E.
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.07.2006
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Summary:This report is the second of a two‐part evaluation of developmental differences in α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐propionic acid receptor (AMPAR) subunit expression in cell populations within white matter and cortex. In part I, we reported that, in rat, developmental expression of Ca2+‐permeable (GluR2‐lacking) AMPARs correlated at the regional and cellular level with increased susceptibility to hypoxia/ischemia (H/I), suggesting an age‐specific role of these receptors in the pathogenesis of brain injury. Part II examines the regional and cellular progression of AMPAR subunits in human white matter and cortex from midgestation through early childhood. Similarly to the case in the rodent, there is a direct correlation between selective vulnerability to H/I and expression of GluR2‐lacking AMPARs in human brain. For midgestational cases aged 20–24 postconceptional weeks (PCW) and for premature infants (25–37 PCW), we found that radial glia, premyelinating oligodendrocytes, and subplate neurons transiently expressed GluR2‐lacking AMPARs. Notably, prematurity represents a developmental window of selective vulnerability for white matter injury, such as periventricular leukomalacia (PVL). During term (38–42 PCW) and postterm neonatal (43–46 PCW) periods, age windows characterized by increased susceptibility to cortical injury and seizures, GluR2 expression was low in the neocortex, specifically on cortical pyramidal and nonpyramidal neurons. This study indicates that Ca2+‐permeable AMPAR blockade may represent an age‐specific therapeutic strategy for potential use in humans. Furthermore, these data help to validate specific rodent maturational stages as appropriate models for evaluation of H/I pathophysiology. J. Comp. Neurol. 497:61–77, 2006. © 2006 Wiley‐Liss, Inc.
Bibliography:National Institute of Neurological Disorders and Stroke - No. NS31718; No. NS38475
Mental Retardation Research Center Grant (National Institute of Child Health and Human Development) - No. P30 HD18655
Epilepsy Foundation
National Institutes of Health - No. HD01359
istex:687A187065DDE03109791CBF880D82C5422D8741
Charles H. Hood Foundation
ArticleID:CNE20978
ark:/67375/WNG-FX2G1K3V-T
William Randolph Hearst Foundation
United Cerebral Palsy Foundation
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.20978