Component
Cellular cyclic AMP accumulation
Cellular cyclic AMP accumulation. Species, exposure and limitations are retained in each linked claim.
2 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
Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"}
- experimental_model
- Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1
- exposure
- A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin
- limitations
- Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed.
- nutrient_topic
- THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
- organism
- Human receptor in CHO cells
- plain_language
- The same receptor can push cAMP up as well as down, and which way depends on which drug is bound.
- primary_references
- [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
- tissue_or_cell_type
- Transfected cells
THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 179–190
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 · source_derived_draft · unverified_draft
### thc-agonist-specific-trafficking Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The same receptor can push cAMP up as well as down, and which way depends on which drug is bound. organism: Human receptor in CHO cells tissue_or_cell_type: Transfected cells experimental_model: Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 limitations: Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed. exposure: A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin evidence_span: {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"} [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
Complete structured claim and evidence
Where it participates (unsigned role)
Cannabinoids inhibited adenylate cyclase in neuroblastoma cell membranes with a pharmacology matching their psychoactivity.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/thc-research/6092901.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "996df269d90c0b0e02d12157d4ebc3dd16e6be5013bc741cf4ed9b798f0e7eb5", "start_char": 0, "end_char": 1329, "text_sha256": "996df269d90c0b0e02d12157d4ebc3dd16e6be5013bc741cf4ed9b798f0e7eb5"}
- experimental_model
- Cannabinoid pharmacology of adenylate cyclase in neuroblastoma cell membranes
- exposure
- Cannabinoid concentration-response on adenylate cyclase
- limitations
- One of the two founding pharmacology papers for Gi coupling. A transformed cell line, and cAMP is a proximal readout.
- nutrient_topic
- THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
- organism
- Cultured neuroblastoma cells
- plain_language
- The drug turns down the enzyme that makes the cell’s main second messenger.
- primary_references
- [thc-p6092901] Cannabinoid inhibition of adenylate cyclase. Pharmacology of the response in neuroblastoma cell membranes. (1984). https://pubmed.ncbi.nlm.nih.gov/6092901/ DOI: 10.1016/s0026-895x(25)15066-9
- tissue_or_cell_type
- Cell membranes
THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 153–164
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cannabinoid pharmacology of adenylate cyclase in neuroblastoma cell membranes · source_derived_draft · unverified_draft
### thc-cannabinoid-inhibits-ac Cannabinoids inhibited adenylate cyclase in neuroblastoma cell membranes with a pharmacology matching their psychoactivity. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The drug turns down the enzyme that makes the cell’s main second messenger. organism: Cultured neuroblastoma cells tissue_or_cell_type: Cell membranes experimental_model: Cannabinoid pharmacology of adenylate cyclase in neuroblastoma cell membranes limitations: One of the two founding pharmacology papers for Gi coupling. A transformed cell line, and cAMP is a proximal readout. exposure: Cannabinoid concentration-response on adenylate cyclase evidence_span: {"source_cache": "artifacts/thc-research/6092901.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "996df269d90c0b0e02d12157d4ebc3dd16e6be5013bc741cf4ed9b798f0e7eb5", "start_char": 0, "end_char": 1329, "text_sha256": "996df269d90c0b0e02d12157d4ebc3dd16e6be5013bc741cf4ed9b798f0e7eb5"} [thc-p6092901] Cannabinoid inhibition of adenylate cyclase. Pharmacology of the response in neuroblastoma cell membranes. (1984). https://pubmed.ncbi.nlm.nih.gov/6092901/ DOI: 10.1016/s0026-895x(25)15066-9
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.