Maya-Vaidya P7: Arbuda An In-Silico Spiking-Network Model of Neuron–Glioma Coupling and Peritumoral Disruption

Version 2 (2026-08-04). Revised to the NLL Universal Paper Format v6. The original text is retained in full; nothing has been deleted. Corrections appear as marked blocks placed at the section that carries the claim, and each one states what the paper said, what the data show, the corrected claim, why it happened, and what still stands. This version adds scoping and resolves three reference placeholders; no claim is retracted.Arms A, B and D are labelled construction-determined by the paper and are now consolidated into an explicit [SCI-10] section: only C/F is an earned result, and it shows that terms I inserted produce the effect those terms encode.The reference list shipped with "[author list to be verified]" placeholders; all three are now resolved. The refractory-period artefact — an apparent 2% → 97% bifurcation that vanished under a physiological control — is given prominent credit as a genuine self-correction. Everything below this line is the original description from version 1. It is retained unchanged for the record. Where it conflicts with the corrections above, the corrections stand. Two framings it repeats have since been withdrawn in full — the Bhaya Quiescence Law and the Buddhi S-Curve. Both are addressed in Maya-Meta P1, now superseded, and in the self-audit of Maya-Meta P2. Maya-Vaidya P7: Arbuda builds the first efficient, fully-interactive spiking-network embodiment of neuron–glioma coupling — wiring a brain-tumour population directly into a cortical microcircuit so the activity→growth relationship can be run, driven, and interrogated live in the browser. The construct is Arbuda (अर्बुद, the classical Sanskrit term for a tumour): a glioma population that listens to the neurons around it through AMPA synapses, so raising local activity raises the tumour's depolarisation-driven growth-signal and lowers it again when that synapse is blocked. The substrate is a leaky integrate-and-fire (LIF) excitatory/inhibitory microcircuit (800 excitatory, 200 inhibitory neurons with conductance-based inhibition) into which 150 non-spiking Arbuda units are wired as postsynaptic AMPA integrators; the proliferation proxy P (time-averaged positive depolarisation of the glioma units) is the readout, and biologically-named levers — excitatory drive, a simulated perampanel AMPA-block, the KCC2 chloride reversal E_Cl, and the neuron→glioma coupling g_AG — are the only controls. Seven experiments across seeds 42/1/7, reproduced bit-for-bit on two machines. Activity drives proliferation: raising drive lifts P monotonically from 0.0 to ~0.040 (Spearman ρ ≈ +1.0), and a simulated perampanel block lowers it monotonically to zero (ρ ≈ −1.0) — model consistency, not clinical efficacy. The tissue beside the tumour runs hotter than tissue far from it (near/far 1.29 fast vs 1.13 slow), and an ablation battery shows this hot zone is causally produced, not geometric: switching off the two peritumoral mechanisms flattens the gradient from 1.41 to exactly 1.00. A coupling-ablation control (g_AG = 0 → P = 0) and a KCC2-loss arm (depolarising E_Cl raises firing, ρ ≈ +1.0) complete the levers. Then an honest ablation of the model's own excitement: an apparent seizure "tipping-point" seen in early runs vanished once neuronal refractoriness was restored, and does not recur across 10 seeds (P(tip) = 0) — reported as a clean null rather than a dramatic cliff. This is the seventh paper in the Maya-Vaidya Series and the first of its Cancer sub-series; no mechanism-level novelty is claimed (neuron–glioma AMPA coupling is established biology), and every finding is treated as a Property, not a Law, per the series meta-protocol Maya-Meta P2 (DOI 10.5281/zenodo.20621503). Honest caveats: results A/B/D are construction-determined (P is defined from depolarisation); the peritumoral gradient is modest and mechanism-dependent; the Arbuda units model only the ~5–10% synaptically-coupled glioma subpopulation; real proliferation is substantially paracrine (NLGN3, BDNF), abstracted here phenomenologically; units are arbitrary and there is no external-data calibration. Scope-lock per Maya-Meta P2: all findings are reproducible signatures within this neuron–glioma architecture, NOT a clinical model of glioma; this work is a research prototype only — it is not a licensed medical device and makes no diagnostic or treatment claim. Series: Part of the Maya-Vaidya Series — neuromorphic AI for clinical neuroscience. India-first. P7 opens the Cancer sub-series. Research prototype only — NOT a licensed medical device. For medical emergencies in India: 112. Links: GitHub Repository | Interactive Dashboard | FAQ | Full Series Index — venky2099.github.io Nexus Learning Labs, Bengaluru · UDYAM-KR-02-0122422 · BHASKAR IN-0526-9452JS · ORCID: 0000-0002-3315-7907 · VAIRAGYA_DECAY_RATE = 0.002315 — an ORCID-derived provenance mark, not an experimental parameter. Each paper's disclosure block states whether it reached a result in that paper. · Canary: MayaNexusVS2026NLL_Bengaluru