Document Detail

Translocation of glutamate transporter subtype excitatory amino acid carrier 1 protein in kainic acid-induced rat epilepsy.
MedLine Citation:
PMID:  12875997     Owner:  NLM     Status:  MEDLINE    
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.
Akiko Furuta; Mami Noda; Satoshi O Suzuki; Yoshinobu Goto; Yoshiko Kanahori; Jeffrey D Rothstein; Toru Iwaki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of pathology     Volume:  163     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-07-23     Completed Date:  2003-09-10     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  779-87     Citation Subset:  AIM; IM    
Department of Neuropathology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
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MeSH Terms
Amino Acid Transport System X-AG / metabolism*
Cell Line
Disease Models, Animal
Epilepsy / chemically induced,  metabolism*
Excitatory Amino Acid Agonists / toxicity*
Excitatory Amino Acid Transporter 3
Glutamate Plasma Membrane Transport Proteins
Glutamic Acid / metabolism*
Kainic Acid
Neurons / cytology,  metabolism
Patch-Clamp Techniques
Rats, Wistar
Receptors, AMPA / metabolism
Receptors, N-Methyl-D-Aspartate / metabolism
Symporters / metabolism*
Reg. No./Substance:
0/Amino Acid Transport System X-AG; 0/Excitatory Amino Acid Agonists; 0/Excitatory Amino Acid Transporter 3; 0/Glutamate Plasma Membrane Transport Proteins; 0/NR1 NMDA receptor; 0/Receptors, AMPA; 0/Receptors, N-Methyl-D-Aspartate; 0/SLC1A1 protein, human; 0/Slc1a1 protein, rat; 0/Symporters; 0/glutamate receptor ionotropic, AMPA 2; 0/glutamate receptor ionotropic, AMPA 3; 487-79-6/Kainic Acid; 56-86-0/Glutamic Acid

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