Differential modulation of human glutamate transporter subtypes by arachidonic acid

Noa Zerangue, Jeffrey L. Arriza, Susan G. Amara, Michael P. Kavanaugh

Research output: Contribution to journalArticlepeer-review

153 Scopus citations


Arachidonic acid has been proposed to be a messenger molecule released following synaptic activation of glutamate receptors and during ischemia. Here we demonstrate that micromolar levels of arachidonic acid inhibit glutamate uptake mediated by EAAT1, a human excitatory amino acid transporter widely expressed in brain and cerebellum, by reducing the maximal transport rate approximately 30%. In contrast, arachidonic acid increased transport mediated by EAAT2, a subtype abundantly expressed in forebrain and midbrain, by causing the apparent affinity for glutamate to increase more than 2-fold. The results demonstrate that the response of different glutamate transporter subtypes to arachidonic acid could influence synaptic transmission and modulate excitotoxicity via positive or negative feedback according to the transporter(s) present in a particular region.

Original languageEnglish
Pages (from-to)6433-6435
Number of pages3
JournalJournal of Biological Chemistry
Issue number12
StatePublished - Mar 24 1995


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