Mt. Akbar et al., EXPRESSION OF GLIAL GLUTAMATE TRANSPORTERS GLT-1 AND GLAST IS UNCHANGED IN THE HIPPOCAMPUS IN FULLY KINDLED RATS, Neuroscience, 78(2), 1997, pp. 351-359
In situ hybridization techniques and quantitative western blotting wer
e used to study the expression of the glial glutamate transporter GLT-
1 and GLAST in the brains of normal (implanted, non-kindled) and fully
kindled rats. Wistar rats were implanted with stimulating electrodes
in the basolateral amygdala, and killed 28 days after the stimulated g
roup had shown stage 5 seizures on five occasions. The brains were pro
cessed for in situ hybridization of messenger RNA for GLT-1 using S-35
-labelled oligonucleotide probes or digoxigenin-labelled riboprobes. P
aired (kindled and non-kindled) sections were used for qualitative and
quantitative analyses. Image analysis of autoradiograms showed no cha
nge in expression of GLT-1 messenger RNA in any region of the hippocam
pus or in the cortex. An increase in expression of GLT-1 messenger RNA
(expressed as percentage difference of control) was observed bilatera
lly in the striatum in kindled animals (16-21%, P<0.05). Nuclear emuls
ion-dipped sections showed predominant glial cell labelling in the hip
pocampus. Particle density analysis revealed reduced cell labelling in
some kindled vs control pairs but overall there was no significant re
duction in labelling in CA1. Equivalent results were found in CA1 usin
g digoxigenin-labelled riboprobes. Quantitative immunoblotting also re
vealed no change in GLT-1 or GLAST transporter protein in the hippocam
pus of kindled animals. From these data we conclude that the enduring
seizure susceptibility associated with the fully kindled state is unli
kely to involve alterations in hippocampal GLT-1 messenger RNA or GLT-
1 and GLAST transporter protein expression. (C) 1997 IBRO. Published b
y Elsevier Science Ltd.