Document Detail


Neonatal loss of gamma-aminobutyric acid pathway expression after human perinatal brain injury.
MedLine Citation:
PMID:  16776375     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECT: Perinatal brain injury leads to chronic neurological deficits in children. Damage to the premature brain produces white matter lesions (WMLs), but the impact on cortical development is less well defined. Gamma-aminobutyric acid(GABA)ergic neurons destined for the cerebral cortex migrate through the developing white matter and form the subplate during late gestation. The authors hypothesized that GABAergic neurons are vulnerable to perinatal systemic insults in premature infants, and that damage to these neurons contributes to impaired cortical development.
METHODS: An immunohistochemical analysis involving markers for oligodendrocytes, GABAergic neurons, axons, and apoptosis was performed on a consecutive series of 15 human neonatal telencephalon samples obtained postmortem from infants born at 25 to 32 weeks of gestation. The tissue samples were divided into two groups based on the presence or absence of WMLs by performing routine histological analyses. The expression of GABAergic neurons was compared between the two groups by using age-matched samples. Two-tailed t-tests were used for statistical analyses. Ten infants had WMLs and five did not. Significant losses of oligodendrocytes and axons and markedly increased apoptosis were appreciated in tissue samples from the infants with WMLs. Samples from infants with WMLs also showed significant losses of glutamic acid decarboxylase-67-positive cells and calretinin-positive cells, shorter neuropeptide Y-positive neurite lengths, and losses of cells expressing GABA(A)alpha1, GABA(B)R1, and N-acetylaspartate diethylamide NR1 receptors when these factors were compared with those in samples from infants without WMLs (all p < 0.02).
CONCLUSIONS: In addition to oligodendrocyte loss, axonal disruption, and excess apoptosis, a significant loss of telencephalon GABAergic neuron expression was found in neonatal brains with WMLs, compared with neonates' brains without WMLs. The loss of GABAergic subplate neurons in infants with WMLs may contribute to the pathogenesis of neurological deficits in children.
Authors:
Shenandoah Robinson; Qing Li; Anne Dechant; Mark L Cohen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of neurosurgery     Volume:  104     ISSN:  0022-3085     ISO Abbreviation:  J. Neurosurg.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-16     Completed Date:  2006-07-18     Revised Date:  2014-09-08    
Medline Journal Info:
Nlm Unique ID:  0253357     Medline TA:  J Neurosurg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  396-408     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Calbindin 2
Case-Control Studies
Caspase 3
Caspases / metabolism
Glutamate Decarboxylase / metabolism
Humans
Hypoxia-Ischemia, Brain / embryology*,  metabolism*,  pathology
Infant, Newborn
Infant, Premature
Isoenzymes / metabolism
Leukomalacia, Periventricular / embryology*,  metabolism*,  pathology
Neuropeptide Y / metabolism
Receptors, GABA / metabolism*
S100 Calcium Binding Protein G / metabolism
gamma-Aminobutyric Acid / metabolism*
Grant Support
ID/Acronym/Agency:
K08 NS046486/NS/NINDS NIH HHS; K08-NS46486-01A1/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/CALB2 protein, human; 0/Calbindin 2; 0/Isoenzymes; 0/Neuropeptide Y; 0/Receptors, GABA; 0/S100 Calcium Binding Protein G; 56-12-2/gamma-Aminobutyric Acid; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases; EC 4.1.1.15/Glutamate Decarboxylase; EC 4.1.1.15/glutamate decarboxylase 1
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