help button home button Am J Pathol PCR Enhanced. PCRboost from Biomatrica
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Furuta, A.
Right arrow Articles by Iwaki, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Furuta, A.
Right arrow Articles by Iwaki, T.
(American Journal of Pathology. 2003;163:779-787.)
© 2003 American Society for Investigative Pathology

Animal Models

Translocation of Glutamate Transporter Subtype Excitatory Amino Acid Carrier 1 Protein in Kainic Acid-Induced Rat Epilepsy

Akiko Furuta*, Mami Noda{dagger}, Satoshi O. Suzuki*, Yoshinobu Goto{ddagger}, Yoshiko Kanahori{dagger}, Jeffrey D. Rothstein§ and Toru Iwaki*

From the Departments of Neuropathology* and Clinical Neurophysiology,{ddagger} Neurological Institute, Graduate School of Medical Sciences, and the Laboratory of Pathophysiology,{dagger} Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan; and the Departments of Neurology and Neuroscience,§ The Johns Hopkins University School of Medicine, Baltimore, Maryland

Abstract

Glutamate excitotoxicity has been implicated in the pathophysiology of epilepsy. Systemic injection of kainic acid (KA) in the rat produces an animal model of human temporal lobe epilepsy. We examined the temporal expression of the sodium-dependent neuronal glutamate transporter, excitatory amino acid carrier 1 (EAAC1), in KA-induced rat epilepsy. As an early alteration, perinuclear deposits of EAAC1 protein were found mainly in the large pyramidal neurons at the hippocampus, neocortex, piriform cortex, and amygdala with the reduction of neuropil staining 6 hours after KA injection. Immunoelectron microscopic study revealed that the perinuclear EAAC1 immunoreactivity corresponded to the translocation to the Golgi complex. At this time point, EAAC1 mRNA was down-regulated. The intracellular aggregation of EAAC1 primarily disappeared by 24 hours. In vitro studies indicated that internalization of EAAC1 from the plasma membrane to the intracellular compartment by KA treatment was associated with the reduction of electrogenic transporter currents. Our results suggest that the transient EAAC1 internalization participates in the modulation of the transporter function preventing excessive glutamate uptake to pyramidal neurons during the early stage of epilepsy.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
Y. Liu, S. Vidensky, A. M. Ruggiero, S. Maier, H. H. Sitte, and J. D. Rothstein
Reticulon RTN2B Regulates Trafficking and Function of Neuronal Glutamate Transporter EAAC1
J. Biol. Chem., March 7, 2008; 283(10): 6561 - 6571.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. Plata, C. R. Sussman, A. Sindic, J. O. Liang, D. B. Mount, Z. M. Josephs, M.-H. Chang, and M. F. Romero
Zebrafish Slc5a12 Encodes an Electroneutral Sodium Monocarboxylate Transporter (SMCTn): A COMPARISON WITH THE ELECTROGENIC SMCT (SMCTe/Slc5a8)
J. Biol. Chem., April 20, 2007; 282(16): 11996 - 12009.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
Y.-X. Yu, L. Shen, P. Xia, Y.-W. Tang, L. Bao, and G. Pei
Syntaxin 1A promotes the endocytic sorting of EAAC1 leading to inhibition of glutamate transport.
J. Cell Sci., September 15, 2006; 119(Pt 18): 3776 - 3787.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the American Society for Investigative Pathology.