Premium
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
Author(s) -
Talos Delia M.,
Follett Pamela L.,
Folkerth Rebecca D.,
Fishman Rachel E.,
Trachtenberg Felicia L.,
Volpe Joseph J.,
Jensen Frances E.
Publication year - 2006
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20978
Subject(s) - subplate , ampa receptor , biology , forebrain , white matter , neuroscience , cerebral cortex , medicine , glutamate receptor , receptor , endocrinology , central nervous system , genetics , radiology , magnetic resonance imaging
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 Ca 2+ ‐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 Ca 2+ ‐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.