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Transient Ischaemia Affects Plasma Membrane Glutamate Transporter, not Vesicular Glutamate Transporter, Expressions in the Gerbil Hippocampus
Author(s) -
Kim D.S.,
Kwak S.E.,
Kim J.E.,
Jung J.Y.,
Won M. H.,
Choi S.Y.,
Kwon O.S.,
Kang T.C.
Publication year - 2006
Publication title -
anatomia, histologia, embryologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.34
H-Index - 35
eISSN - 1439-0264
pISSN - 0340-2096
DOI - 10.1111/j.1439-0264.2005.00677.x
Subject(s) - glutamate receptor , gerbil , excitatory amino acid transporter , transporter , ischemia , hippocampus , excitotoxicity , glutamate aspartate transporter , extracellular , biology , medicine , chemistry , endocrinology , pharmacology , biochemistry , receptor , gene
Summary In the present study, we investigated expressions of vesicular glutamate transporter (VGLUT) and of the plasma membrane glutamate transporters [glutamate transporter 1 (GLT‐1), glutamate/aspartate transporter (GLAST) and excitatory amino acid carrier 1 (EAAC‐1)] in the gerbil hippocampus following transient ischaemia. The expressional levels and distribution patterns of VGLUT immunoreactivities were unaltered until 3 days after ischaemic‐insults. However, VGLUT‐2 immunoreactivity in the CA1 region was reduced at 4 days after ischaemia due to delayed neuronal death. In addition, both GLT‐1 and GLAST immunoreactivities in the CA1 region were enhanced at 30 min – 12 h after ischaemia‐reperfusion and their expression began to reduce at 24 h after ischaemia‐reperfusion. In contrast, EAAC‐1 immunoreactivity was transiently reduced in the CA1 region at 30 min after ischaemia, re‐enhanced at 3–12 h after ischaemia, and re‐reduced at 24 h after ischaemia. These findings suggest that malfunctions of plasma membrane glutamate transporters, not of VGLUT, may play an important role in the elevation of extracellular glutamate concentration following ischaemic insults.