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Altered long-term potentiation in the hippocampus of apolipoprotein E-deficient mice.

Authors
Veinbergs, I; Jung, MW; Young, SJ; Van Uden, E; Groves, PM; Masliah, E
Citation
Neuroscience letters, 249(2-3):71-74, 1998
Journal Title
Neuroscience letters
ISSN
0304-39401872-7972
Abstract
Recent studies suggest that apolipoprotein E (apoE) plays a neurotrophic role in the central nervous system and that an aberrant function of this molecule might result in neurodegeneration. Supporting this notion, apoE-deficient mice show neurodegenerative and cognitive alterations. To characterize physiological changes associated with synaptic damage and cognitive impairment in apoE-deficient mice, we investigated synaptic plasticity in the hippocampus of urethane anesthetized mice. Electrical stimulation was delivered to the perforant pathway and the resulting evoked field excitatory postsynaptic potential (EPSP) and population spike were recorded in the hilus. Long-term potentiation, as measured in the population spike, was reduced by 50% in apoE-deficient mice when compared to wild-type controls. In contrast, there were no significant differences in the evoked field EPSP between wild-type and apoE-deficient mice following high-frequency stimulation. These results support the notion that cognitive impairment and synaptic loss in the hippocampus of apoE-deficient mice might be associated with impaired long-term potentiation.
MeSH terms
AnimalsApolipoproteins E/genetics/*physiologyBrain MappingExcitatory Postsynaptic PotentialsHippocampus/*physiology*Long-Term PotentiationMiceMice, Inbred C57BLMice, Knockout
PMID
9682819
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
정, 민환
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