Document Detail


Loss of cation-chloride cotransporter expression in preterm infants with white matter lesions: implications for the pathogenesis of epilepsy.
MedLine Citation:
PMID:  20467335     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epilepsy associated with preterm birth is often refractory to anticonvulsants. Children who are born preterm are also prone to cognitive delay and behavioral problems. Brains from these children often show diffuse abnormalities in cerebral circuitry that is likely caused by disrupted development during critical stages of cortical formation. To test the hypothesis that prenatal injury impairs the developmental switch of gamma-amino butyric acid (GABA)ergic synapses from excitatory to inhibitory, thereby disrupting cortical circuit formation and predisposing to epilepsy, we used immunohistochemistry to compare the expression of cation-chloride transporters that developmentally regulate postsynaptic GABAergic discharges in postmortem cerebral samples from infants born preterm with known white matter injury (n = 11) with that of controls with minimal white matter gliosis (n = 7). Controls showed the expected developmental expression of cation-chloride transporters NKCC1 and KCC2 and ofcalretinin, a marker of a GABAergic neuronal subpopulation. Samples from infants with white matter damage showed a significant loss of expression of both NKCC1 and KCC2 in subplate and white matter. By contrast, there were no significant differences in total cell number or glutamate transporter VGLUT1 expression. Together, these novel findings suggest a molecular mechanism involved in the disruption of a critical stage of cerebral circuit development after brain injury from preterm birth that may predispose to epilepsy.
Authors:
Shenandoah Robinson; Irina Mikolaenko; Ian Thompson; Mark L Cohen; Monisha Goyal
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of neuropathology and experimental neurology     Volume:  69     ISSN:  1554-6578     ISO Abbreviation:  J. Neuropathol. Exp. Neurol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-31     Completed Date:  2010-06-14     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  2985192R     Medline TA:  J Neuropathol Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  565-72     Citation Subset:  IM    
Affiliation:
Divisions of Pediatric Neurosurgery, Neurology, Rainbow Babies & Children's Hospital, 11100 Euclid Ave, Cleveland, OH 44106, USA. Shenandoah.robinson@uhhs.com
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MeSH Terms
Descriptor/Qualifier:
Brain / metabolism*,  pathology
Calcium-Binding Protein, Vitamin D-Dependent / metabolism*
Cell Count
Female
Gliosis / metabolism,  pathology
Humans
Immunohistochemistry
Infant, Newborn
Infant, Premature
Leukoencephalopathies / metabolism*,  pathology
Male
Nerve Fibers, Myelinated / metabolism*,  pathology
Sodium-Potassium-Chloride Symporters / metabolism*
Symporters / metabolism*
Grant Support
ID/Acronym/Agency:
R01 NS060765/NS/NINDS NIH HHS; R01 NS060765-03/NS/NINDS NIH HHS; T35 HL082544/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Protein, Vitamin D-Dependent; 0/Sodium-Potassium-Chloride Symporters; 0/Symporters; 0/calretinin; 0/potassium-chloride symporters
Comments/Corrections

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