The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits.

The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Research Abstract Details 

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The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Abstract Text:

Hans Peter Koch,Ronald Lane Brown,Hans Peter Larsson,

Excitatory amino acid transporters (EAATs) use sodium and potassium gradients to remove glutamate from the synapse and surrounding extracellular space, thereby sustaining efficient synaptic transmission and maintaining extracellular glutamate concentrations at subneurotoxic levels. In addition to sodium-driven glutamate uptake, EAATs also mediate a glutamate-activated chloride conductance via a channel-like mechanism. EAATs are trimeric proteins and are thought to comprise three identical subunits. Previous studies have shown that the sodium-driven uptake of glutamate occurs independently in each of the three subunits. In contrast, a recent study reports high Hill coefficients for the activation of EAAT anion currents by glutamate and suggests that the subunits function cooperatively in gating the chloride conductance. In the present work, we find that the Hill coefficient for the activation of the anion current by glutamate is approximately 1 in both EAAT3 and EAAT4. Furthermore, we also used fluorescent labeling and inactivation correlation on EAAT3 and EAAT4 to determine whether the glutamate-activated chloride conductance is gated independently or cooperatively by the transporters. We found that both glutamate uptake currents and glutamate-activated chloride currents are mediated independently by each subunit of an EAAT multimer. It has been suggested that EAAT subtypes with particularly large anion conductances can directly influence the excitability of presynaptic terminals in certain neurons. Thus, the finding that the anion conductance is gated independently, rather than cooperatively, is important because it significantly alters predictions of the influence that EAAT-mediated anion currents will have on synaptic transmission at low glutamate concentrations.

The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Publishing Authors By Initials

HP Koch,RL Brown,HP Larsson,

For similar animals: chordata: vertebrates: amphibia: anura: pipidae: xenopus: xenopus laevis research abstracts see: animals: chordata: vertebrates: amphibia: anura: pipidae: xenopus: xenopus laevis research

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The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 2943-7

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 14

MONTH: Mar

YEAR: 2007

The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8102140

The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Keywords Mesh Terms:

KEYWORDS: Xenopus laevis

MESH TERMS: physiology

Chemical & Substance for Abstract: The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits. Information

Substance Name: Glutamic Acid

Registry Number: 56-86-0

Grant and Affiliation Information for The glutamate-activated anion conductance in excitatory amino acid transporters is gated independently by the individual subunits.

AFFILIATION: Neurological Sciences Institute, Oregon Health & Science University, Beaverton, Oregon 97006, USA.

Country: United States

AGENCY: United States NINDS

GRANT: T32-NS045553

ACRONYM: NS

MEDLINETA: J Neurosci

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