Component

Mouse metabotropic glycine receptor / Gpr158

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

3 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 it acts on

  1. Bath glycine at 1 mM increased layer-II/III prefrontal neuronal excitability in control mice but not Gpr158-knockout mice under synaptic receptor blockade.

    Mouse metabotropic glycine receptor / Gpr158 → Glycine-evoked mouse prefrontal neuronal excitability source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse acute slices, intrinsic-current measurements and knockout comparison.
    limitations
    High bath exposure; absence of effect in layer V reinforces cell-type specificity.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    This receptor can make selected neurons more excitable.
    primary_references
    Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 250–256

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse acute slices, intrinsic-current measurements and knockout comparison. · source_derived_draft · unverified_draft

    ## glycine-gpr158-cortex This receptor can make selected neurons more excitable. Bath glycine at 1 mM increased layer-II/III prefrontal neuronal excitability in control mice but not Gpr158-knockout mice under synaptic receptor blockade. Model: Mouse acute slices, intrinsic-current measurements and knockout comparison. Limitations: High bath exposure; absence of effect in layer V reinforces cell-type specificity. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Blocking PKA or ERK signaling suppressed the glycine-associated increase in medium-spiny-neuron excitability; ERK and Kv7.2 serine phosphorylation increased in the study.

    PKA/ERK signaling in mouse accumbens neurons → Glycine-sensitive excitability in mouse accumbens neurons source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse slice pharmacological inhibition and phosphorylation assays.
    limitations
    Associated phosphorylation and inhibitor effects do not establish every kinase-substrate step; cholinergic interneurons did not share the firing response.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    The channel response depends on intracellular signaling steps.
    primary_references
    Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38884814/ · DOI 10.1007/s00018-024-05260-w

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 266–272

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse slice pharmacological inhibition and phosphorylation assays. · source_derived_draft · unverified_draft

    ## glycine-gpr158-kinase-dependence The channel response depends on intracellular signaling steps. Blocking PKA or ERK signaling suppressed the glycine-associated increase in medium-spiny-neuron excitability; ERK and Kv7.2 serine phosphorylation increased in the study. Model: Mouse slice pharmacological inhibition and phosphorylation assays. Limitations: Associated phosphorylation and inhibitor effects do not establish every kinase-substrate step; cholinergic interneurons did not share the firing response. Evidence access: Primary full text Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38884814/ · DOI 10.1007/s00018-024-05260-w
    Complete structured claim and evidence

  2. In mouse accumbens slices, 1 mM glycine increased medium-spiny-neuron firing and reduced M-current amplitude; a selective M-current inhibitor mimicked and occluded the response.

    Glycine → Potassium M-current in mouse accumbens medium spiny neurons source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Male C57BL/6J mice aged four to six weeks; slice patch clamp with synaptic blockers.
    limitations
    Authors attributed the response to GPR158; pharmacology alone is weaker than a receptor-knockout test and does not prove direct channel binding.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Glycine-sensitive signaling intersects with potassium-channel control of firing.
    primary_references
    Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38884814/ · DOI 10.1007/s00018-024-05260-w

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 258–264

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male C57BL/6J mice aged four to six weeks; slice patch clamp with synaptic blockers. · source_derived_draft · unverified_draft

    ## glycine-gpr158-potassium-current Glycine-sensitive signaling intersects with potassium-channel control of firing. In mouse accumbens slices, 1 mM glycine increased medium-spiny-neuron firing and reduced M-current amplitude; a selective M-current inhibitor mimicked and occluded the response. Model: Male C57BL/6J mice aged four to six weeks; slice patch clamp with synaptic blockers. Limitations: Authors attributed the response to GPR158; pharmacology alone is weaker than a receptor-knockout test and does not prove direct channel binding. Evidence access: Primary full text Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38884814/ · DOI 10.1007/s00018-024-05260-w
    Complete structured claim and evidence

In the sources

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

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards