Glutamate Clearance
Glutamate Clearance - Related Videos
04:10
Analyzing the Glutamate Release and Clearance at a Single Neuron Synapse in a Mouse Brain Slice
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2025
This video demonstrates evaluating glutamate release and clearance at single corticostriatal synapses in a mouse brain slice. Electrical stimulation facilitates glutamate release at the synapse. The released glutamate alters sensor protein's fluorescence, which decays over time, indicating release and clearance efficiency.
09:42
Deriving the Time Course of Glutamate Clearance with a Deconvolution Analysis of Astrocytic Transporter Currents
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Cited by 11 •
2013
We describe an analytical method to estimate the lifetime of glutamate at astrocytic membranes from electrophysiological recordings of glutamate transporter currents in astrocytes.
10:46
Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models
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Cited by 15 •
2017
Here, we describe the setup, software navigation, and data analysis for a spatially and temporally precise method of measuring tonic and phasic extracellular glutamate changes in vivo using enzyme-linked microelectrode arrays (MEA).
01:09
Hepatic Drug Clearance: Restrictive and Nonrestrictive Clearance
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2025
Hepatic clearance refers to the volume of blood cleared of a drug by the liver per unit of time. It plays a crucial role in drug metabolism and elimination. While hepatic clearance is commonly estimated by subtracting renal clearance from total body clearance, other pathways, such as pulmonary or biliary clearance, may also contribute. However, these pathways are generally less significant than hepatic and renal clearance. Most drugs undergo restrictive clearance, which is proportional to the...
07:48
Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina
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Cited by 16 •
2015
With this study, we introduce a standardized stress model for the isolated superfused bovine retina for future preclinical therapeutic testing. The effect of either hypoxia (pure N2) or glutamate stress (250 µM glutamate) on retinal function represented by a- and b-wave amplitudes was evaluated.
FAQs
Excitatory amino acid transporters rapidly remove glutamate after its release, limiting how long the neurotransmitter remains available to influence nearby cells. Transporters on both astrocytes and neurons contribute to this control. Their activity therefore affects the duration and strength of excitatory communication, helping prevent signaling from becoming excessive while preserving appropriate transmission within neural circuits.
Astrocytes do more than remove glutamate from the synaptic environment. They convert taken-up glutamate into glutamine, which can return to neurons and support regeneration of glutamate through the glutamate–glutamine cycle. This cooperation links transmitter removal with recycling, allowing neurons and astrocytes to share responsibility for maintaining excitatory neurotransmission over repeated signaling events.
Inefficient clearance allows glutamate-related stimulation to persist or become excessive. Because clearance normally limits signaling and protects neurons from overactivation, impaired transporter function can promote excitotoxicity, a damaging effect associated with excessive stimulation. This connection makes transport activity important not only for normal synaptic communication but also for understanding mechanisms of neuronal injury.
The speed and effectiveness of removal help determine how long glutamate can act after synaptic release. Faster or more efficient clearance restricts the persistence of excitatory signaling, whereas reduced efficiency can prolong or intensify its effects. Consequently, clearance is a regulatory component of neural circuit function rather than merely a disposal step after neurotransmitter release.
Researchers can examine the activity of excitatory amino acid transporters on astrocytes and neurons, the conversion of glutamate to glutamine, and the return of glutamine to neurons. They can also relate these processes to changes in signaling strength, timing, and neuronal protection. Together, these observations connect cellular transport and recycling with broader circuit-level function.
The cycle provides a framework for understanding how excitatory neurotransmission is sustained while glutamate is simultaneously removed from synaptic regions. Astrocyte processing and neuronal reuse connect local synaptic events with ongoing circuit activity. Studying this relationship can clarify how neural communication is maintained and how disruptions in recycling may alter neurotransmission.
These conditions are relevant because disrupted glutamate transport or recycling can disturb the balance between effective signaling and excessive stimulation. In epilepsy, stroke, and neurodegenerative disease research, investigators can use clearance mechanisms to examine how altered neurotransmission may contribute to neuronal stress or injury. The process therefore links synaptic physiology with disease-related changes in neural tissue.