Linked Life Data

12626441

Source:http://linkedlifedata.com/resource/pubmed/id/12626441

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-5-1
pubmed:abstractText
The effects of neonatal dexamethasone (DEX) treatment on spatial learning and hippocampal synaptic plasticity were investigated in adult rats. Spatial learning in reference and working memory versions of the Morris maze was impaired in DEX-treated rats. In hippocampal slices of DEX rats, long-term depression was facilitated and potentiation was impaired. Paired-pulse facilitation was normal, suggesting a postsynaptic defect as cause of the learning and plasticity deficits. Western blot analysis of hippocampal postsynaptic densities (PSD) revealed a reduction in NR2B subunit protein, whereas the abundance of the other major N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A), AMPA receptor subunits (GluR2/3), scaffolding proteins, and Ca2+/calmodulin-dependent protein kinase II (alphaCaMKII) were unaltered. This selective reduction in NR2B likely resulted from altered receptor assembly rather than subunit expression, because the abundance of NR2B in the homogenate and crude synaptosomal fractions was unaltered. In addition, the activity of alphaCaMKII, an NMDA receptor complex associated protein kinase, was increased in PSD of DEX rats. The results indicate that neonatal treatment with DEX causes alterations in composition and function of the hippocampal NMDA receptor complex that persist into adulthood. These alterations likely explain the deficits in hippocampal synaptic plasticity and spatial learning induced by neonatal DEX treatment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
911-3
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12626441-Animals, pubmed-meshheading:12626441-Animals, Newborn, pubmed-meshheading:12626441-Calcium-Calmodulin-Dependent Protein Kinase Type 2, pubmed-meshheading:12626441-Calcium-Calmodulin-Dependent Protein Kinases, pubmed-meshheading:12626441-Dexamethasone, pubmed-meshheading:12626441-Enzyme Activation, pubmed-meshheading:12626441-Glucocorticoids, pubmed-meshheading:12626441-Hippocampus, pubmed-meshheading:12626441-Long-Term Potentiation, pubmed-meshheading:12626441-Long-Term Synaptic Depression, pubmed-meshheading:12626441-Maze Learning, pubmed-meshheading:12626441-Neuronal Plasticity, pubmed-meshheading:12626441-Rats, pubmed-meshheading:12626441-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:12626441-Spatial Behavior, pubmed-meshheading:12626441-Synaptic Transmission
pubmed:year
2003
pubmed:articleTitle
Long-lasting effects of neonatal dexamethasone treatment on spatial learning and hippocampal synaptic plasticity: involvement of the NMDA receptor complex.
pubmed:affiliation
Department of Pharmacology and Anatomy, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
pubmed:publicationType
Journal Article