Component
Extracellular D-aspartate in mouse prefrontal cortex
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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
Oral D-aspartate at 20 mM in drinking water for one month and a separate 500 mg/kg intraperitoneal exposure increased extracellular prefrontal D-aspartate in mice.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Mouse microdialysis; chronic oral and separate acute injection conditions.
- limitations
- Water concentration is not a fixed mg/kg dose; human brain exposure remains unmeasured here.
- nutrient_topic
- D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
- plain_language
- Both tested routes changed the brain extracellular pool in mice.
- primary_references
- Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 216–222
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse microdialysis; chronic oral and separate acute injection conditions. · source_derived_draft · unverified_draft
## d-aspartate-brain-exposure Both tested routes changed the brain extracellular pool in mice. Oral D-aspartate at 20 mM in drinking water for one month and a separate 500 mg/kg intraperitoneal exposure increased extracellular prefrontal D-aspartate in mice. Model: Mouse microdialysis; chronic oral and separate acute injection conditions. Limitations: Water concentration is not a fixed mg/kg dose; human brain exposure remains unmeasured here. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidenceFour weeks of olanzapine at 5 mg/kg/day intraperitoneally increased prefrontal extracellular D-aspartate and glutamate in wild-type mice; the increments were absent in Ddo-knockout mice.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Mouse microdialysis 24 hours after the final injection.
- limitations
- Knockouts already differ at baseline. This does not prove the pathway mediates clinical antipsychotic efficacy.
- nutrient_topic
- D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
- plain_language
- Removing the enzyme removed this drug-associated increment in the mouse experiment.
- primary_references
- Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 280–286
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse microdialysis 24 hours after the final injection. · source_derived_draft · unverified_draft
## d-aspartate-olanzapine-mouse-dependence Removing the enzyme removed this drug-associated increment in the mouse experiment. Four weeks of olanzapine at 5 mg/kg/day intraperitoneally increased prefrontal extracellular D-aspartate and glutamate in wild-type mice; the increments were absent in Ddo-knockout mice. Model: Mouse microdialysis 24 hours after the final injection. Limitations: Knockouts already differ at baseline. This does not prove the pathway mediates clinical antipsychotic efficacy. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
The events it takes part in
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Situations it appears in
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In the sources
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Open hypotheses
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This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.