First-pass extracted concept

glutamatergic neurotransmission

Candidate: concept label3 source documents4 linked claims

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Evidence Snippets

The web research summary states that the anchor paper explicitly reports glutamatergic neurotransmission for sugar-triggered transmission.

Evidence 1Source 1DOI PubMedprovenance

PubMed/PMC text confirms major themes including glutamatergic neurotransmission, epidemiology, and gene-environment interplay.

Evidence 2Source 2DOI PubMedprovenance

Therapies that target glutamatergic neurotransmission are available, but many have met with difficulty because of untoward adverse effects.

Evidence 3Source 3DOI PubMedprovenance

Supporting Sources

Source 1primary paper2022Nature NeuroscienceDOI PubMed

1 evidence snippet 1 linked claim Claim 1

Source 2review2016The LancetDOI PubMed

1 evidence snippet 1 linked claim Claim 1

Source 3review2015Cold Spring Harbor Perspectives in MedicineDOI PubMed

1 evidence snippet 2 linked claims Claim 1 Claim 2

Linked Claims

Claim 1mechanismsupports2022Source 1DOI PubMed

The paper reports differential purinergic versus glutamatergic neurotransmission in gut sensor cell signaling.

Quoted textsource-backed

The key mechanistic anchors for downstream extraction are ... differential purinergic versus glutamatergic neurotransmission.

Claim 2review scope summarysupports2016Source 2DOI PubMed

The review frames schizophrenia as shaped by converging human genetics, neurodevelopment, glutamatergic synapse biology, and epidemiologic or environmental risk factors.

Claim 3disease link summarysupports2015Source 3DOI PubMed

Evidence points to a shared glutamate pathology for epilepsy and other central nervous system disorders including depression.

Claim 4pathophysiology summarysupports2015Source 3DOI PubMed

Seizures induce elevations in extracellular glutamate that contribute to excitotoxic damage.