Component
Rat hippocampal local glutamate supply for release
Context-specific entity; species, compartment and exposure are stated on each claim.
4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Repeated high-frequency stimulation of rat hippocampal and cortical terminals reduced synaptic efficacy and glutamate release; the effect depended on activity pattern.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat brain slices with axons transected; alternating 20 Hz and 0.2 Hz stimulation and naturalistic patterns.
- limitations
- This is a local experimental supply limitation, not a dietary glutamate-deficiency threshold.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- A local transmitter supply can become insufficient when demand rises.
- primary_references
- A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 130–136
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat brain slices with axons transected; alternating 20 Hz and 0.2 Hz stimulation and naturalistic patterns. · source_derived_draft · unverified_draft
## glutamate-recycling-demand A local transmitter supply can become insufficient when demand rises. Repeated high-frequency stimulation of rat hippocampal and cortical terminals reduced synaptic efficacy and glutamate release; the effect depended on activity pattern. Model: Rat brain slices with axons transected; alternating 20 Hz and 0.2 Hz stimulation and naturalistic patterns. Limitations: This is a local experimental supply limitation, not a dietary glutamate-deficiency threshold. Evidence access: Primary full text A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
Complete structured claim and evidenceAdding 500 micromolar glutamine prevented or reversed the activity-dependent loss of glutamate-mediated synaptic responses in the tested rat slices.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Rat hippocampal/cortical slices with high-frequency stimulation, with or without prior enzyme inhibition.
- limitations
- Bath addition of glutamine is not oral L-glutamate treatment or proof of improved human cognition.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- Providing a usable precursor bypassed part of the local synthesis limitation.
- primary_references
- A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 146–152
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat hippocampal/cortical slices with high-frequency stimulation, with or without prior enzyme inhibition. · source_derived_draft · unverified_draft
## glutamate-recycling-glutamine-rescue Providing a usable precursor bypassed part of the local synthesis limitation. Adding 500 micromolar glutamine prevented or reversed the activity-dependent loss of glutamate-mediated synaptic responses in the tested rat slices. Model: Rat hippocampal/cortical slices with high-frequency stimulation, with or without prior enzyme inhibition. Limitations: Bath addition of glutamine is not oral L-glutamate treatment or proof of improved human cognition. Evidence access: Primary full text A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
Complete structured claim and evidenceAt 0.2 Hz, evoked responses remained stable for 60 minutes despite prior glutamine-synthetase inhibition in the rat slice experiment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Rat hippocampal slices; matched low-frequency recording control.
- limitations
- This limited period of preserved function does not make glutamine synthesis dispensable.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- A stored reserve can hide a supply defect when demand is low.
- primary_references
- A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 154–160
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat hippocampal slices; matched low-frequency recording control. · source_derived_draft · unverified_draft
## glutamate-recycling-low-demand A stored reserve can hide a supply defect when demand is low. At 0.2 Hz, evoked responses remained stable for 60 minutes despite prior glutamine-synthetase inhibition in the rat slice experiment. Model: Rat hippocampal slices; matched low-frequency recording control. Limitations: This limited period of preserved function does not make glutamine synthesis dispensable. Evidence access: Primary full text A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
Complete structured claim and evidence
Where it participates (unsigned role)
Blocking glutamine synthetase with methionine sulfoximine worsened activity-dependent synaptic depression in rat hippocampal slices.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Rat slice glutamine-synthetase inhibition and evoked field-potential recordings.
- limitations
- The inhibitor also restricts newly synthesized glutamine; recycling is not the only possible affected source.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- Disabling the recycling enzyme made the local supply problem worse.
- primary_references
- A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 138–144
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat slice glutamine-synthetase inhibition and evoked field-potential recordings. · source_derived_draft · unverified_draft
## glutamate-recycling-gs-block Disabling the recycling enzyme made the local supply problem worse. Blocking glutamine synthetase with methionine sulfoximine worsened activity-dependent synaptic depression in rat hippocampal slices. Model: Rat slice glutamine-synthetase inhibition and evoked field-potential recordings. Limitations: The inhibitor also restricts newly synthesized glutamine; recycling is not the only possible affected source. Evidence access: Primary full text A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24559677/ · DOI 10.1016/j.neuron.2013.12.026
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.