Component

Mouse serotonin receptor 4 / Htr4

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. Htr4 knockout or receptor antagonism removed the secretory response to tryptamine.

    Mouse serotonin receptor 4 / Htr4 → Mouse colonic ionic and fluid secretion after tryptamine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse knockout and pharmacological blockade.
    limitations
    Not a universal receptor requirement for every action of tryptamine.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The metabolite could not produce this response without its receptor.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 570–576

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout and pharmacological blockade. · source_derived_draft · unverified_draft

    ## tryptophan-htr4-loss The metabolite could not produce this response without its receptor. Htr4 knockout or receptor antagonism removed the secretory response to tryptamine. Model: Mouse knockout and pharmacological blockade. Limitations: Not a universal receptor requirement for every action of tryptamine. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Tryptamine increased epithelial ionic flux and colonoid fluid secretion through 5-HT4 receptors in mice.

    Tryptamine → Mouse colonic ionic and fluid secretion after tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Germ-free and human-stool-colonized mouse tissue/colonoids.
    limitations
    Humanized microbiota does not make the host tissue human.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A microbial tryptophan product can change intestinal fluid movement.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 562–568

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Germ-free and human-stool-colonized mouse tissue/colonoids. · source_derived_draft · unverified_draft

    ## tryptophan-tryptamine-secretion A microbial tryptophan product can change intestinal fluid movement. Tryptamine increased epithelial ionic flux and colonoid fluid secretion through 5-HT4 receptors in mice. Model: Germ-free and human-stool-colonized mouse tissue/colonoids. Limitations: Humanized microbiota does not make the host tissue human. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    Complete structured claim and evidence

  2. Colonizing germ-free mice with B. thetaiotaomicron engineered to produce tryptamine accelerated gastrointestinal transit.

    Tryptamine → Mouse gastrointestinal transit after microbial tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Engineered bacterium in gnotobiotic mice.
    limitations
    Not evidence that tryptophan supplements have the same effect in humans.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Changing microbial production changed movement through the gut.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 578–584

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Engineered bacterium in gnotobiotic mice. · source_derived_draft · unverified_draft

    ## tryptophan-tryptamine-transit Changing microbial production changed movement through the gut. Colonizing germ-free mice with B. thetaiotaomicron engineered to produce tryptamine accelerated gastrointestinal transit. Model: Engineered bacterium in gnotobiotic mice. Limitations: Not evidence that tryptophan supplements have the same effect in humans. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    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