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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1998-7-27
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pubmed:abstractText |
Using apolipoprotein E knockout mice derived from the Maeda source [Piedrahita J. A. et al. (1992) Proc. natn. Acad Sci. US.A. 89, 4471 4475], we have studied the influence of apolipoprotein E gene deletion on normal CNS function by neurological tests and water maze learning, hippocampal ultrastructure assessed by quantitative immunocytochemistry and electron microscopy, CNS plasticity, i.e. hippocampal long-term potentiation and amygdaloid kindling, and CNS repair, i.e. synaptic recovery in the hippocampus following deafferentation. In each study there was little difference between the apolipoprotein E knockout mice and wild-type controls of similar age and genetic background. Apolipoprotein E knockout mice aged eight months demonstrated accurate spatial learning and normal neurological function. Synaptophysin and microtubule-associated protein 2 immunohistochemistry and electron microscopic analysis of these animals revealed that the hippocampal synaptic and dendritic densities were similar between genotypes. The induction and maintenance of kindled seizures and hippocampal long-term potentiation were indistinguishable between groups. Finally, unilateral entorhinal cortex lesions produced a marked loss of hippocampal synaptophysin immunoreactivity in both groups and a marked up-regulation of apolipoprotein E in the wild-type group. Both apolipoprotein E knockout and wild-type groups showed immunohistochemical evidence of reactive synaptogenesis, although the apolipoprotein E knockout group may have initially shown greater synaptic loss. It is suggested that either apolipoprotein E is of no importance in the maintenance of synaptic integrity and in processes of CNS plasticity and repair, or more likely, alternative (apolipo)proteins may compensate for the loss of apolipoprotein E in the knockout animals.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0306-4522
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pubmed:author |
pubmed-author:AndersonRR,
pubmed-author:BarneyJ AJA,
pubmed-author:BlissT VTV,
pubmed-author:CainD PDP,
pubmed-author:CambonKK,
pubmed-author:DaviesH AHA,
pubmed-author:ErringtonM LML,
pubmed-author:FellowsL ALA,
pubmed-author:GrayR ARA,
pubmed-author:HigginsG AGA,
pubmed-author:HonRR,
pubmed-author:LargeC HCH,
pubmed-author:StewartMM
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pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
93-110
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9607706-Animals,
pubmed-meshheading:9607706-Apolipoproteins E,
pubmed-meshheading:9607706-Behavior, Animal,
pubmed-meshheading:9607706-Dentate Gyrus,
pubmed-meshheading:9607706-Electrophysiology,
pubmed-meshheading:9607706-Entorhinal Cortex,
pubmed-meshheading:9607706-GAP-43 Protein,
pubmed-meshheading:9607706-Hippocampus,
pubmed-meshheading:9607706-Immunohistochemistry,
pubmed-meshheading:9607706-Kindling, Neurologic,
pubmed-meshheading:9607706-Mice,
pubmed-meshheading:9607706-Mice, Knockout,
pubmed-meshheading:9607706-Microtubule-Associated Proteins,
pubmed-meshheading:9607706-Neurons,
pubmed-meshheading:9607706-Synapses,
pubmed-meshheading:9607706-Synaptophysin
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pubmed:year |
1998
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pubmed:articleTitle |
Behavioural, physiological and morphological analysis of a line of apolipoprotein E knockout mouse.
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pubmed:affiliation |
Neuroscience Unit, Glaxo Wellcome Research and Development, Medicines, Research Centre, Stevenage, Herts, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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