Reading the workbench assumptions and output dependencies
Read the explanation
This video explains the saved program, not established medical outcomes. Its baseline assigns network modularity zero point six eight and entropy one point one two. At the native peak preset, its effect multiplier is one, and the arithmetic gives zero point six eight minus zero point five eight, or zero point one zero. Entropy becomes one point one two plus one point nine five, or three point zero seven. The bars use five hundred pixels per modularity unit. These numbers are authored model assumptions, not patient measurements. The twenty four hour branch computes its percentage as thirty eight times the activation input divided by one hundred, times a compound multiplier and its normalized input. With the saved default activation of eighty eight percent and multiplier one, rounding thirty three point four four gives thirty three percent. Changing the activation control to zero gives zero percent. The bars use eight pixels per percentage point: two hundred sixty four pixels versus zero. This is a mathematical control dependency in the program, not evidence of biological growth. Now inspect the late time branch critically. It assigns a score of seven directly, independent of those control values. Setting the input to zero gives zero modeled growth, but the displayed score remains seven. So the remission label is a branch assignment, not a fitted or validated clinical forecast. The JSON download preserves the inputs and computed fields, making that dependency visible. The receptor ratio and glutamate controls are exported, but neither enters this metric calculation. Treat all medical accuracy as unverified and use this draft to understand the saved implementation.
Understanding the 5-MeO-DMT Neurobiology & Remission Model
How does this workbench model receptor kinetics, network entropy, and TrkB-driven dendritic plasticity, and what are its computational limits?
This interactive workbench illustrates a conceptual model linking 5-MeO-DMT pharmacology to depression remission across cellular and network levels. In the code, receptor binding triggers three sequential phases: acute network disintegration (reducing Default Mode Network modularity Q while increasing Shannon entropy H), a subacute neuroplastic window driven by tropomyosin receptor kinase B (TrkB) and mTOR signaling where cortical pyramidal neurons sprout new dendritic spines, and a day 14+ sustained remission state. However, the modularity, entropy, spine density, and MADRS depression scores are computed via simplified mathematical scaling functions rather than an empirically fitted biophysical whole-brain simulation.
The workbench relies on hardcoded algebraic scaling formulas rather than clinical trial readouts or biophysical ODE networks. Output scores such as MADRS = 7 and modularity Q = 0.32 are illustrative presets rather than patient-level diagnostic predictions. While peer-reviewed in vitro and in vivo studies confirm that serotonergic psychoplastogens promote spinogenesis through TrkB and mTOR pathways, clinical symptom remission rates from survey literature reflect open naturalistic observations rather than Phase III confirmatory trials.
Try a worked example
At default baseline (T = 0 minutes), click the '2. Acute 5-MeO-DMT Peak (10 min)' preset button (or the '10 min' timeline button). The timeline scrubs to 10 minutes, the brain network canvas transitions to show widespread inter-network edges, DMN Modularity (Q) drops from 0.68 to 0.10, Neural Entropy increases from 1.12 b to 3.07 b, and the simulated MADRS score decreases from 34 to 14.
TrkB and mTOR-Mediated Structural Plasticity
The simulation's cortical dendritic spine visualizer reflects the psychoplastogenic mechanism where psychedelics stimulate prefrontal pyramidal arborization and spinogenesis. Preclinical research demonstrates that classical psychedelics promote neuritogenesis, spinogenesis, and functional synaptogenesis in cortical neurons through TrkB receptor activation and downstream mTOR signaling, effects blocked by TrkB antagonist ANA-12 or mTOR inhibitor rapamycin. Psychedelics Promote Structural and Functional Neural Plasticity - PMC
In the workbench's 24-hour window, spine density growth is calculated directly as a function of the TrkB activation force slider and administered dose. While the real biological cascade involves complex intracellular protein translation and AMPA receptor trafficking, this educational model abstracts that cascade into a proportional outgrowth percentage.
Network Disintegration and Clinical Heuristics
The network visualizer models the hypothesis that potent serotonergic agonism transiently disrupts rigid intra-network connectivity in the Default Mode Network (mPFC and PCC), promoting cross-network functional repertoire and higher Shannon signal diversity during acute subjective peak effects.
The workbench's clinical audit references epidemiological and naturalistic findings where synthetic 5-MeO-DMT or toad secretion inhalation was associated with self-reported reductions in depression and anxiety. Users should note that observational surveys and mechanistic simulations demonstrate biological plausibility but do not substitute for formal clinical psychiatric evaluation or regulatory drug validation.
Verifies that serotonergic psychedelics promote neuritogenesis, spinogenesis, and synaptogenesis in cortical neurons via TrkB- and mTOR-dependent signaling pathways.