Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/131913
Title: Species differences in the distribution of the glutamate receptor subunit, GluR1, in the rat and monkey entorhinal cortex.
Authors: He, Y.
Ong, W.Y. 
Leong, S.K. 
Keywords: Alzheimer's disease
Entorhinal cortex
GluR1
Monkey
Rat
Temporal cortex
Issue Date: 1997
Citation: He, Y., Ong, W.Y., Leong, S.K. (1997). Species differences in the distribution of the glutamate receptor subunit, GluR1, in the rat and monkey entorhinal cortex.. Journal für Hirnforschung 38 (1) : 27-33. ScholarBank@NUS Repository.
Abstract: The distribution of the DL-alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) receptor subunits GluR1 and GluR2/3 were studied by immunocytochemistry in the rat and monkey temporal neocortex and entorhinal cortex. The monkey neocortex was similar to the rat neo- and entorhinal cortex, in that non-pyramidal neurons were densely labelled for GluR1, while pyramidal neurons were lightly labelled. The monkey entorhinal cortex was very different, in that dense GluR1 labelling was present in the pyramidal neurons of layer V. Although many GluR2/3-positive pyramidal neurons were also present in layers II, III, V and VI of the monkey entorhinal cortex, the neuropilar staining in layer V was less intense for GluR2/3, than for GluR1. This suggests that there were fewer GluR2 or GluR3 subunits in that layer compared with GluR1, and it is possible that many of the GluR1 subunits exist as homomers. Since GluR1 homomeric channels are permeable to calcium ions and are inwardly rectifying, the high GluR1 content of the layer V pyramidal neurons could render these cells particularly susceptible to calcium influx, and consequently, calcium-mediated neuronal injury. This could therefore be one of the reasons why the entorhinal cortex shows some of the earliest and most severe pathological alterations in Alzheimer's disease.
Source Title: Journal für Hirnforschung
URI: http://scholarbank.nus.edu.sg/handle/10635/131913
ISSN: 00218359
Appears in Collections:Staff Publications

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