A Model of High Affinity Glutamic Acid Transport by Rat Cortical Synaptosomes–a Refinement of the Originally Proposed Model

Dd, Wheeler

doi:10.1111/j.1471-4159.1979.tb09918.x

Cited by 43 publications

(11 citation statements)

References 9 publications

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“…Lineweaver-Burk plots at each of the sodi um concentrations used (except for [Na] = 0) are linear (25,28). Both the intercept and tire slopes of the lines change with [Na], Thus, both Va and Kt are functions of the [Na].…”

mentioning

confidence: 99%

“…Numerous simplifications of the above model were fitted to the data (25,28). For glutamic acid, dropping any part of the model resulted in a substantially higher error in the model fit.…”

Section: Minimal Best Fit Modelmentioning

confidence: 99%

“…A summary of the results of studies of glutamic acid and GABA transport follows. The methods used in these studies have been described in detail, and will therefore not be presented here (23,25,27,28). For GABA, a family of curves of similar shape results; each of the curves shows the expected tendency to saturate at high GABA concentra tions as the velocity approaches Va. For glu tamic acid, the shape of the curve changes with [Na]; the curve for 120.8 mM sodium saturates much faster than the other curves and falls below the curve for 43 mM at a [Gj of about 6 X 1GTSM From these plots, we can already make certain statements about the sodium dependence.…”

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confidence: 99%

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A Model for GABA and Glutamic Acid Transport by Cortical Synaptosomes

Dd¹

1980

Pharmacology

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confidence: 99%

“…Numerous simplifications of the above model were fitted to the data (25,28). For glutamic acid, dropping any part of the model resulted in a substantially higher error in the model fit.…”

Section: Minimal Best Fit Modelmentioning

confidence: 99%

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confidence: 99%

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A Model for GABA and Glutamic Acid Transport by Cortical Synaptosomes

Dd¹

1980

Pharmacology

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“…When [Na+]i is high, on the other hand, the carrier will stay longer in the state where it can rebind glutamate (because Na+ can rebind before the carrier conformation changes to one that cannot rebind Na+ or glutamate), and raising the intracellular glutamate concentration will inhibit uptake. Similarly, Wheeler (1979) concluded that, at the external face, at least some of the sodium binds before glutamate. Kanner & Bendahan (1982) propose a reaction scheme similar to that shown in Fig.…”

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confidence: 99%

Electrogenic uptake of glutamate and aspartate into glial cells isolated from the salamander (Ambystoma) retina.

Barbour

Brew

Attwell

1991

The Journal of Physiology

186

166

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SUMMARY1. The effects of excitatory amino acids on the membrane current of isolated retinal glial cells (Muller cells) were investigated using whole-cell patch clamping.2. L-Glutamate evoked an inward current at membrane potentials between -140 and +50 mV. The current was larger at more negative potentials.3. The glutamate-evoked current was activated by external cations with relative efficacies: Na+ > Li+> K+ > Cs+, choline. It was activated by internal cations with relative efficacies K+ > Rb+ > Cs+ > choline. Chloride and divalent cations did not affect the glutamate-evoked current.4. Raising the intracellular sodium or glutamate concentrations, or raising the extracellular potassium concentration, reduced the current evoked by external glutamate. The suppressive effect of internal glutamate was larger when the internal sodium concentration was high.5. Some analogues of glutamate also evoked an inward current. Responses to Laspartate resembled those to glutamate, but for aspartate the apparent affinity was higher and the voltage dependence of the current was steeper. In the physiological potential range the current evoked by a saturating dose of aspartate was less than that evoked by a saturating dose of glutamate.6. The uptake blocker threo-3-hydroxy-DL-aspartate (30,tM) reduced the glutamate-evoked current, but also generated a current itself. Dihydrokainate (510 /LM) weakly inhibited the glutamate-evoked current without generating a current itself.7. The commonly used blockers of glutamate-gated ion channels, 2-amino-5-phosphonovalerate (APV; 100 ,M), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20 /bM), and kynurenate (1 mM) had no effect on the glutamate-evoked current. 8. The voltage dependence, cation dependence and pharmacological profile of the current evoked by excitatory amino acids indicate that it is caused by activation of the high-affinity glutamate uptake carrier. This carrier appears to transport one glutamate anion into the cell, one K+ ion out of the cell, and two or more Na+ ions into the cell, on each carrier cycle. At the inner membrane surface some or all of the transported Na+ dissociates from the carrier after the transported glutamate has dissociated.MS 8441

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“…Transport processes play a critical role in the synaptic function of the putative amino acid neurotransmitters, since they are necessary for inactivation of transmitter following stimulus-induced release (Krnjevic, 1974;Roberts et al, 1976). Extensive kinetic studies of the high affinity transport of GABA and glutamic acid in rat brain synaptosomes have been carried out in this laboratory (Wheeler, 1979(Wheeler, a, b, 1981Hollingsworth, 1978, 1979;Wheeler, Wise, and Callihan, 1980). Initial velocity of uptake has been measured as a function of both sodium and amino acid concentration, and computer optimization techniques used to fit these data to each of several plausible models.…”

Section: Introductionmentioning

confidence: 98%

Effect of hyperbaric oxygen on GABA transport in rat brain synaptosomes

Wheeler

Blackburn

Tai

1983

J. Neural Transmission

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Initial velocities of uptake of GABA have been measured in rat brain synaptosomes from animals which had been exposed to oxygen at high pressure (OHP) and compared to similar measurements in normobaric controls. For hypothalamus, no changes in GABA uptake occurred subsequent to exposure to OHP. For cortical synaptosomes, however, exposure to OHP resulted in a decreased velocity of GABA uptake at all combinations of [Na] and [GABA] used. The OHP data were found to fit the same transport model as found previously for control data. Thus, OHP exposure did not alter the basic mechanism by which sodium and GABA interact with the carrier in the process of transport. However, the constants which quantitate the model were changed by OHP exposure. As a consequence, the several kinetic parameters which are calculated from the model change in the OHP animals. These kinetic parameters are compared to similar calculations for both normobaric control animals and normobaric aged animals. Although the effects of OHP do not precisely parallel the effects of aging, the alterations in kinetic parameters are in several ways similar in the aged and OHP animals.

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A Model of High Affinity Glutamic Acid Transport by Rat Cortical Synaptosomes–a Refinement of the Originally Proposed Model

Cited by 43 publications

References 9 publications

A Model for GABA and Glutamic Acid Transport by Cortical Synaptosomes

A Model for GABA and Glutamic Acid Transport by Cortical Synaptosomes

Electrogenic uptake of glutamate and aspartate into glial cells isolated from the salamander (Ambystoma) retina.

Effect of hyperbaric oxygen on GABA transport in rat brain synaptosomes

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