Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0306-4522(96)00608-2
Title: Differential expression of apolipoprotein D and apolipoprotein E in the kainic acid-lesioned rat hippocampus
Authors: Ong, W.-Y. 
He, Y.
Suresh, S.
Patel, S.C.
Keywords: Apolipoprotein D
Apolipoprotein E
Excitotoxin
Hippocampus
Kainic acid
Neurodegeneration
Issue Date: 12-May-1997
Source: Ong, W.-Y., He, Y., Suresh, S., Patel, S.C. (1997-05-12). Differential expression of apolipoprotein D and apolipoprotein E in the kainic acid-lesioned rat hippocampus. Neuroscience 79 (2) : 359-367. ScholarBank@NUS Repository. https://doi.org/10.1016/S0306-4522(96)00608-2
Abstract: Expression of apolipoprotein D, a member of the lipocalin superfamily of transporter proteins, was investigated in the kainic acid-lesioned rat hippocampus. Using an anti-rat apolipoprotein D antibody and biotin-avidin-enhanced immunocytochemistry, in the normal rat hippocampus there was little apolipoprotein D expression, that was restricted mainly to scattered astrocytes. By contrast, kainic acid-injected rats showed apolipoprotein D immunoreactivity in the pyramidal neurons of the affected CA fields 24-48 h after injection of the excitotoxin, at a time when there was no histological evidence of cell death. Apolipoprotein D immunoreactivity peaked by day 3, coincident with neuronal cell death, and declined thereafter, reaching very low levels by day 7. Besides pyramidal neurons, apolipoprotein D immunoreactivity was also observed in a small number of reactive glial cells in the affected CA fields, but not in the vascular compartments at any time-point. In contrast to the neuronal expression of apolipoprotein D, apolipoprotein E immunoreactivity was observed predominantly in degenerating astrocytes. In conclusion, following excitotoxic injury with kainic acid, apolipoprotein D is expressed in hippocampal pyramidal neurons destined for subsequent cell death.
Source Title: Neuroscience
URI: http://scholarbank.nus.edu.sg/handle/10635/120734
ISSN: 03064522
DOI: 10.1016/S0306-4522(96)00608-2
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