Component
Synaptic-like microvesicles of the beta cell
Synaptic-like microvesicles of the beta cell. Species, exposure and limitations are retained in each linked 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.
Where it participates (unsigned role)
Rat beta-cells release GABA by calcium-dependent exocytosis of synaptic-like microvesicles and the GABA thus released can diffuse over sufficient distances within the islet interstitium to activate GABA-A receptors in neighboring cells, confocal immunocytochemistry revealed the presence of GABA-A receptors in glucagon-secreting alpha-cells but not in beta- and delta-cells with transcripts of alpha1, alpha4 and beta1-3 subunits detected in purified alpha-cells but not in beta-cells, the antagonist SR95531 increased glucagon secretion at 1 millimolar glucose twofold and completely abolished the inhibitory action of 20 millimolar glucose on glucagon release, and basal and glucose-stimulated secretion of insulin and somatostatin were unaffected.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/15047619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1f64e75f4c5822ecc05331804e4d127c8b1702249327c4ed85fa07d96898d5b0", "start_char": 0, "end_char": 1478, "text_sha256": "1f64e75f4c5822ecc05331804e4d127c8b1702249327c4ed85fa07d96898d5b0"}
- experimental_model
- Confocal immunocytochemistry, transcript analysis, whole-cell voltage clamp and hormone secretion with a receptor antagonist
- exposure
- Endogenous GABA released from beta cells, with the GABA-A antagonist SR95531 and the calcium channel blocker isradipine
- limitations
- The antagonist experiment is what makes this causal for the endogenous signal. Receptor detection was by immunocytochemistry and transcripts in purified cells.
- nutrient_topic
- GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
- organism
- Rat
- plain_language
- Block the receptor and glucose stops switching off glucagon entirely, and the receptor is on the glucagon cell and not on the insulin cell.
- primary_references
- [gb-p15047619] Glucose inhibition of glucagon secretion from rat alpha-cells is mediated by GABA released from neighboring beta-cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15047619/ DOI: 10.2337/diabetes.53.4.1038
- tissue_or_cell_type
- Purified islet cells and intact islets
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Confocal immunocytochemistry, transcript analysis, whole-cell voltage clamp and hormone secretion with a receptor antagonist · source_derived_draft · unverified_draft
### gb-the-receptor-is-on-the-alpha-cell-only Rat beta-cells release GABA by calcium-dependent exocytosis of synaptic-like microvesicles and the GABA thus released can diffuse over sufficient distances within the islet interstitium to activate GABA-A receptors in neighboring cells, confocal immunocytochemistry revealed the presence of GABA-A receptors in glucagon-secreting alpha-cells but not in beta- and delta-cells with transcripts of alpha1, alpha4 and beta1-3 subunits detected in purified alpha-cells but not in beta-cells, the antagonist SR95531 increased glucagon secretion at 1 millimolar glucose twofold and completely abolished the inhibitory action of 20 millimolar glucose on glucagon release, and basal and glucose-stimulated secretion of insulin and somatostatin were unaffected. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: Block the receptor and glucose stops switching off glucagon entirely, and the receptor is on the glucagon cell and not on the insulin cell. organism: Rat tissue_or_cell_type: Purified islet cells and intact islets experimental_model: Confocal immunocytochemistry, transcript analysis, whole-cell voltage clamp and hormone secretion with a receptor antagonist limitations: The antagonist experiment is what makes this causal for the endogenous signal. Receptor detection was by immunocytochemistry and transcripts in purified cells. exposure: Endogenous GABA released from beta cells, with the GABA-A antagonist SR95531 and the calcium channel blocker isradipine evidence_span: {"source_cache": "artifacts/gaba-research/15047619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1f64e75f4c5822ecc05331804e4d127c8b1702249327c4ed85fa07d96898d5b0", "start_char": 0, "end_char": 1478, "text_sha256": "1f64e75f4c5822ecc05331804e4d127c8b1702249327c4ed85fa07d96898d5b0"} [gb-p15047619] Glucose inhibition of glucagon secretion from rat alpha-cells is mediated by GABA released from neighboring beta-cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15047619/ DOI: 10.2337/diabetes.53.4.1038
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.