What question did this study set out to answer?

To determine the role of glutamate transporters in regulating extracellular glutamate levels and identify the source of extracellular glutamate during transporter inhibition.

July 20, 1999Proceedings of the National Academy of SciencesOpen Access

Inhibition of uptake unmasks rapid extracellular turnover of glutamate of nonvesicular origin

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Authors

DJDenis JabaudonUniversity of Geneva KSKeiko ShimamotoSuntory Foundation for Life Sciences YYY. Yasuda‐Kamatani

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Overview

Experimental study demonstrates rapid nonvesicular glutamate accumulation in hippocampal slices after uptake inhibition, indicating transporters constantly balance basal release.

Key Points

To determine the role of glutamate transporters in regulating extracellular glutamate levels and identify the source of extracellular glutamate during transporter inhibition.
Applied the non-transportable glutamate uptake inhibitor DL-threo-beta-benzyloxyaspartate (TBOA) to organotypic hippocampal slice cultures.
Monitored extracellular glutamate changes using NMDA receptors on patched CA3 hippocampal neurons as biosensors in the presence of tetrodotoxin, clostridial toxins, and glutamine synthase inhibitors.
TBOA application provoked a rapid increase in extracellular glutamate concentration that was Ca2+-independent, persisted during action potential blockade with tetrodotoxin, and was unaffected by clostridial toxin inhibition of vesicular release.
Inhibition of glutamine synthase accelerated extracellular glutamate accumulation, demonstrating that glial stores provide nonvesicular glutamate, while TBOA effectively blocked synaptically evoked astrocyte transporter currents without inducing heteroexchange.

Cite This Study

Jabaudon et al. (1999) studied this question.

synapsesocial.com/papers/6a9e7d22000dfce5919bc2fd https://doi.org/10.1073/pnas.96.15.8733

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July 20, 1999Proceedings of the National Academy of SciencesOpen Access

Inhibition of uptake unmasks rapid extracellular turnover of glutamate of nonvesicular origin

View Full Paper

Ask AI

Bookmark

Authors

DJDenis JabaudonUniversity of Geneva KSKeiko ShimamotoSuntory Foundation for Life Sciences YYY. Yasuda‐Kamatani

Discussion

Member takes

Overview

Experimental study demonstrates rapid nonvesicular glutamate accumulation in hippocampal slices after uptake inhibition, indicating transporters constantly balance basal release.

Key Points

To determine the role of glutamate transporters in regulating extracellular glutamate levels and identify the source of extracellular glutamate during transporter inhibition.
Applied the non-transportable glutamate uptake inhibitor DL-threo-beta-benzyloxyaspartate (TBOA) to organotypic hippocampal slice cultures.
Monitored extracellular glutamate changes using NMDA receptors on patched CA3 hippocampal neurons as biosensors in the presence of tetrodotoxin, clostridial toxins, and glutamine synthase inhibitors.
TBOA application provoked a rapid increase in extracellular glutamate concentration that was Ca2+-independent, persisted during action potential blockade with tetrodotoxin, and was unaffected by clostridial toxin inhibition of vesicular release.
Inhibition of glutamine synthase accelerated extracellular glutamate accumulation, demonstrating that glial stores provide nonvesicular glutamate, while TBOA effectively blocked synaptically evoked astrocyte transporter currents without inducing heteroexchange.

Cite This Study

Jabaudon et al. (1999) studied this question.

synapsesocial.com/papers/6a9e7d22000dfce5919bc2fd https://doi.org/10.1073/pnas.96.15.8733

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