Component
Potassium M-current in mouse accumbens medium spiny neurons
Context-specific entity; species, compartment and exposure are stated on each claim.
1 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
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.
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
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.