Document Detail


A novel model for prenatal brain damage. II. Long-term deficits in hippocampal cell number and hippocampal-dependent behavior following neonatal GABAA receptor activation.
MedLine Citation:
PMID:  12781999     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Premature infants are at especially high risk for asphyxia, seizures, and other conditions that cause hypoxia-ischemia. These events result in abnormal brain pathology and behavioral deficits that persist throughout adolescence and into adulthood. Current rodent models of human infant hypoxic-ischemic brain damage have focused on exogenous glutamate receptor agonist exposure in the postnatal day 7 rat. While this model is considered analogous to the newborn human, no adequate models for preterm infant brain damage have been developed. Recent work from our lab has proposed a potential model for preterm infant brain damage in which neonatal rats are treated with exogenous muscimol, the selective gamma-aminobutyric acid(A) (GABA(A)) receptor agonist, on postnatal days 0 and 1. In the companion paper to this one (Exp. Neurol., in press), we report fewer neurons in the hippocampal formation on postnatal day 7 (6 days after treatment), but the persistence of these anatomical deficits, and potential resultant behavioral dysfunctions, were not investigated. In the current experiment, we documented that muscimol exposure on postnatal days 0 and 1 leads to fewer neurons in the male and female rat hippocampus (CA1, CA2/3, and dentate gyrus) on postnatal day 21. Also, neonatal muscimol exposed males and females displayed deficits on hippocampal-dependent learning tasks such as a preweanling version of the Morris water maze task and the open field task. We conclude that exposure to exogenous GABA(A) receptor activation over the first 2 days of postnatal life, a model for preterm infant hypoxic injury, produces anatomical and behavioral deficits observed into adolescence.
Authors:
Joseph L Nuñez; Jesse J Alt; Margaret M McCarthy
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Experimental neurology     Volume:  181     ISSN:  0014-4886     ISO Abbreviation:  Exp. Neurol.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-03     Completed Date:  2003-08-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370712     Medline TA:  Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  270-80     Citation Subset:  IM    
Affiliation:
Physiology Department, University of Maryland School of Medicine, Baltimore 21201, USA. jnune001@umaryland.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Behavior, Animal
Body Weight
Brain Damage, Chronic / chemically induced,  pathology*,  physiopathology*
Cell Count
Chronic Disease
Disease Models, Animal
Female
GABA Agonists
Hippocampus / drug effects,  pathology*,  physiopathology*
Male
Maze Learning
Muscimol
Organ Size
Rats
Rats, Sprague-Dawley
Receptors, GABA-A / agonists,  metabolism*
Spatial Behavior
Time
Grant Support
ID/Acronym/Agency:
R01 MH 52716/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/GABA Agonists; 0/Receptors, GABA-A; 2763-96-4/Muscimol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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