Do extracellular glutamate levels depend on vesicular release of glutamate?
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Extracellular glutamate levels are influenced by vesicular release mechanisms. Studies suggest that glutamate release can occur through full fusion of vesicles with the membrane or via 'kiss-and-run' mechanisms, where glutamate is released through a fusion pore . During brain ischemia, the cystine/glutamate antiporter plays a crucial role in elevating extracellular glutamate levels, leading to neuronal damage through overactivation of extrasynaptic NMDA receptors . Research on cultured neurons indicates that glutamate release can deplete vesicular stores, with sustained release dependent on Ca2+ levels and vesicular mechanisms . Furthermore, vesicular filling of glutamate, removal of Synapsin I, and Ca2+-dependent exocytosis are key steps in the release process . Additionally, satellite glial cells have been shown to release glutamate in a calcium-dependent manner, with potential modulation by botulinum neurotoxin type A .
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| Papers (5) | Insight |
|---|---|
| Yes, extracellular glutamate levels depend on vesicular release from satellite glial cells, which can be modulated by Botulinum neurotoxin type A (BoNTA) as shown in the study. | |
| Yes, extracellular glutamate levels depend on vesicular release as glutamate is specifically accumulated into synaptic vesicles, supporting its role as a major excitatory neurotransmitter. | |
8 Citations | Yes, extracellular glutamate levels depend on vesicular release mechanisms, as shown in hippocampal neurons in culture, where vesicular exocytosis is the dominant route for glutamate depletion. |
7 Citations | Extracellular glutamate levels depend on vesicular release, with approximately half of glutamate release utilizing the proton gradient between the vesicle and synaptic cleft, suggesting significant 'kiss-and-run' release. |
| Not addressed in the paper. |
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