Component

Mouse NMDA-type receptors, subunits unresolved

Context-specific entity; species, compartment and exposure are stated on each claim.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Ddo deletion increased NMDA-evoked currents and membrane GluN1/GluN2A in mouse nigral dopamine neurons.

    Mouse D-aspartate oxidase / Ddo → Mouse NMDA-type receptors, subunits unresolved source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Ddo-knockout mouse substantia-nigra neurons.
    limitations
    Region-specific knockout response; not a universal change after oral supplementation.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Prolonged higher D-aspartate was accompanied by receptor remodeling.
    primary_references
    Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 200–206

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ddo-knockout mouse substantia-nigra neurons. · source_derived_draft · unverified_draft

    ## d-aspartate-ddo-loss-nmdar Prolonged higher D-aspartate was accompanied by receptor remodeling. Ddo deletion increased NMDA-evoked currents and membrane GluN1/GluN2A in mouse nigral dopamine neurons. Model: Ddo-knockout mouse substantia-nigra neurons. Limitations: Region-specific knockout response; not a universal change after oral supplementation. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
    Complete structured claim and evidence

  2. Glycine increased opening frequency of NMDA-activated channels in cultured mouse brain neurons, with potentiation detected at 10 nM.

    Glycine → Mouse NMDA-type receptors, subunits unresolved source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse cultured neurons and outside-out patch recordings.
    limitations
    The effect was distinct from strychnine-sensitive glycine receptors; it does not define an oral glycine or glutamate response.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    An amino acid usually associated with inhibition can assist an excitatory receptor.
    primary_references
    Glycine potentiates the NMDA response in cultured mouse brain neurons. · 1987 · https://pubmed.ncbi.nlm.nih.gov/2433595/ · DOI 10.1038/325529a0

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 234–240

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cultured neurons and outside-out patch recordings. · source_derived_draft · unverified_draft

    ## glutamate-nmda-glycine An amino acid usually associated with inhibition can assist an excitatory receptor. Glycine increased opening frequency of NMDA-activated channels in cultured mouse brain neurons, with potentiation detected at 10 nM. Model: Mouse cultured neurons and outside-out patch recordings. Limitations: The effect was distinct from strychnine-sensitive glycine receptors; it does not define an oral glycine or glutamate response. Evidence access: Primary abstract Glycine potentiates the NMDA response in cultured mouse brain neurons. · 1987 · https://pubmed.ncbi.nlm.nih.gov/2433595/ · DOI 10.1038/325529a0
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Persistent D-aspartate elevation after Ddo deletion accompanied increased extracellular glutamate, active caspases, reactive glia and age-dependent brain abnormalities.

    Mouse D-aspartate oxidase / Ddo → Age-dependent brain pathology after mouse Ddo deletion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Constitutive Ddo-knockout mice studied across age.
    limitations
    Genetic lifelong exposure is not equivalent to a short human supplement course.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Long-term loss of clearance had adverse outcomes despite some short-term signaling effects.
    primary_references
    d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 248–254

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Constitutive Ddo-knockout mice studied across age. · source_derived_draft · unverified_draft

    ## d-aspartate-chronic-loss-aging Long-term loss of clearance had adverse outcomes despite some short-term signaling effects. Persistent D-aspartate elevation after Ddo deletion accompanied increased extracellular glutamate, active caspases, reactive glia and age-dependent brain abnormalities. Model: Constitutive Ddo-knockout mice studied across age. Limitations: Genetic lifelong exposure is not equivalent to a short human supplement course. Evidence access: Primary abstract d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
    Complete structured claim and evidence

  2. Aged Ddo-knockout mice showed reduced synaptic GluN1/GluN2B, altered plasticity and greater vulnerability to phencyclidine-related prepulse-inhibition deficits.

    Mouse D-aspartate oxidase / Ddo → Synaptic NMDA receptor availability in mouse hippocampus source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Aging Ddo-knockout mouse hippocampus and behavior.
    limitations
    Different age/region/endpoint from nigral GluN1/GluN2A increases; recorded as context, not a wording correction.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Receptor adaptation can reverse the apparent direction of an earlier signaling effect.
    primary_references
    d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 256–262

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Aging Ddo-knockout mouse hippocampus and behavior. · source_derived_draft · unverified_draft

    ## d-aspartate-chronic-loss-receptors Receptor adaptation can reverse the apparent direction of an earlier signaling effect. Aged Ddo-knockout mice showed reduced synaptic GluN1/GluN2B, altered plasticity and greater vulnerability to phencyclidine-related prepulse-inhibition deficits. Model: Aging Ddo-knockout mouse hippocampus and behavior. Limitations: Different age/region/endpoint from nigral GluN1/GluN2A increases; recorded as context, not a wording correction. Evidence access: Primary abstract d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
    Complete structured claim and evidence

  3. Ddo deletion or oral D-aspartate elevation enhanced hippocampal LTP without improving cognitive flexibility in the reported mouse experiments.

    D-Aspartate → Mouse hippocampal long-term potentiation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse genetic and oral-exposure models; slices and behavioral tests.
    limitations
    LTP is not synonymous with better memory; oral dose not specified in accessed abstract.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    A stronger synaptic-plasticity signal did not translate into a general cognitive advantage.
    primary_references
    Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility. · 2008 · https://pubmed.ncbi.nlm.nih.gov/17981050/ · DOI 10.1016/j.mcn.2007.09.012

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 240–246

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic and oral-exposure models; slices and behavioral tests. · source_derived_draft · unverified_draft

    ## d-aspartate-ltp A stronger synaptic-plasticity signal did not translate into a general cognitive advantage. Ddo deletion or oral D-aspartate elevation enhanced hippocampal LTP without improving cognitive flexibility in the reported mouse experiments. Model: Mouse genetic and oral-exposure models; slices and behavioral tests. Limitations: LTP is not synonymous with better memory; oral dose not specified in accessed abstract. Evidence access: Primary abstract Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility. · 2008 · https://pubmed.ncbi.nlm.nih.gov/17981050/ · DOI 10.1016/j.mcn.2007.09.012
    Complete structured claim and evidence

  4. D-aspartate excited mouse nigral dopamine neurons with NMDA, AMPA and metabotropic receptor-sensitive components.

    D-Aspartate → Excitatory responses of mouse substantia-nigra dopamine neurons source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse substantia nigra pars compacta slice electrophysiology.
    limitations
    Antagonist-sensitive responses do not by themselves prove direct agonism at every receptor; indirect glutamate release can contribute.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Several receptor pathways contribute to the observed electrical response.
    primary_references
    Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 192–198

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse substantia nigra pars compacta slice electrophysiology. · source_derived_draft · unverified_draft

    ## d-aspartate-nigral-excitation Several receptor pathways contribute to the observed electrical response. D-aspartate excited mouse nigral dopamine neurons with NMDA, AMPA and metabotropic receptor-sensitive components. Model: Mouse substantia nigra pars compacta slice electrophysiology. Limitations: Antagonist-sensitive responses do not by themselves prove direct agonism at every receptor; indirect glutamate release can contribute. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
    Complete structured claim and evidence

  5. D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect.

    D-Aspartate → Glutamate release from mouse cortical synaptosomes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA.
    limitations
    This is evoked release under transporter blockade, not basal release in an intact human brain.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Receptor-sensitive feedback changed release under an uptake-blocked assay condition.
    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 232–238

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA. · source_derived_draft · unverified_draft

    ## d-aspartate-terminal-glutamate Receptor-sensitive feedback changed release under an uptake-blocked assay condition. D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect. Model: Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA. Limitations: This is evoked release under transporter blockade, not basal release in an intact human brain. 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

  6. EAAT inhibition strongly potentiated D-aspartate-evoked, but not L-aspartate-evoked, currents in Ddo-knockout mouse neurons.

    EAAT inhibition in mouse nigral neurons → Excitatory responses of mouse substantia-nigra dopamine neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Ddo-knockout mouse nigral neuron transporter-blocker experiments.
    limitations
    A protective adaptation is an interpretation; human transporter failure and dietary consequences were not tested.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Uptake can buffer excitation when breakdown is impaired.
    primary_references
    Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 208–214

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ddo-knockout mouse nigral neuron transporter-blocker experiments. · source_derived_draft · unverified_draft

    ## d-aspartate-uptake-buffer Uptake can buffer excitation when breakdown is impaired. EAAT inhibition strongly potentiated D-aspartate-evoked, but not L-aspartate-evoked, currents in Ddo-knockout mouse neurons. Model: Ddo-knockout mouse nigral neuron transporter-blocker experiments. Limitations: A protective adaptation is an interpretation; human transporter failure and dietary consequences were not tested. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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    Evidence, AI assistance and curation standards