Maya-Vaidya P8: Srava A Dual-Channel Spiking Model of Synaptic and Paracrine Neuron–Glioma Coupling, and the Activity-Scaled Residual Under AMPA Blockade

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 corrects a contradiction between the Discussion and the Limitations.The Discussion states the 93% paracrine floor "is not a property of our particular parameter choices: it is coverage." It is. Coverage sets reach; the magnitude is a gain ratio — re-running at half the paracrine gain moves the headline from 92.9% to 87.2% and the drive-scaled floors from 96.3/94.0/90.5% to 94.6/89.1/83.0%.The reach result (100% vs 14.7%) is a genuine geometric statement and stands. The additivity null is disclosed as a unit test on a defined sum. 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 Two framings it repeats have since been withdrawn in full — the Bhaya Quiescence Law and the Buddhi S-Curve. Both are addressed in Maya-Meta P1, now superseded, and in the self-audit of Maya-Meta P2.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 P8: Srava asks what happens when you close only one of a tumour’s two doors. Its predecessor, Maya-Vaidya P7 (Arbuda, DOI 10.5281/zenodo.21489850), wired a glioma population into a spiking cortical microcircuit through the electrical door — fast glutamate (AMPA) synapses — and stated plainly that its single largest abstraction was the omission of paracrine signalling. That omission is this paper’s subject. The construct is Srava (स्राव; secretion, outflow): the chemical channel, in which neuronal activity drives ADAM10-mediated shedding of neuroligin-3 into the tumour microenvironment (Venkatesh 2015, 2017 — where Nlgn3 knockout abolishes xenograft growth outright, making this route rate-limiting rather than merely contributory), thrombospondin-1 promotes neuron–glioma synaptogenesis and tracks survival (Krishna 2023), and BDNF acting on TrkB traffics AMPA receptors to the glioma membrane so the neurogliomal synapse potentiates with use (Taylor 2023). The substrate is P7’s leaky integrate-and-fire circuit — 800 excitatory / 200 inhibitory neurons with conductance-based inhibition — plus 150 non-spiking glioma units of which only ~15% carry a fast AMPA synapse, a deliberately sparse wiring reflecting the ~5–10% synaptically-coupled subpopulation observed experimentally. Onto this we add a reaction–diffusion paracrine field (secretion proportional to local firing, diffusion, clearance; suppressible by an ADAM10-like lever) that drives growth in every glioma unit regardless of synapse, and a bounded use-dependent potentiation of the synapse. Proliferation is decomposed into its two sources, P = P_syn + P_para. Seven experiments, seeds 42/1/7, reproduced bit-for-bit on two machines, ~34 s on a laptop CPU. (1) Both channels are activity-driven, and the paracrine channel grows synapse-free cells (0 → 0.046; ρ ≈ +1.0). (2) Decomposition: P_syn 0.0018 versus P_para 0.0376 — the field carries 95% of population growth, though per wired cell the synaptic channel is substantial (0.0123). (3) The central result. Full simulated perampanel blockade does not return growth to baseline: it plateaus at a paracrine floor retaining ~93% of the proxy (0.045 → 0.042), and the height of that floor rises with neuronal activity — 0.014, 0.040, 0.045 at drive 1.0, 1.4, 1.8, against a no-activity baseline of 0. (4) Monotherapy versus combination: untreated 0.045 → perampanel 0.042 → ADAM10-like 0.003 → combination 0.000; each lever removes its own channel and leaves the other. (5) BDNF potentiation strengthens the wired coupling to 1.30× and stays bounded. (6) Reach supplies the mechanism: the field grows 100% of glioma units, the sparse synapse 14.7%. (7) Two pre-registered negatives, reported with equal prominence: the combination is purely additive (measured synergy 0.6% of untreated growth) — so the case for combining is channel coverage, not synergy, and we decline the word synergy; and the field shows no tumour-centred halo (near/far 1.03, essentially uniform), a negative about our own construction that bounds the spatial claims the model can support. No biological novelty is claimed: activity-driven NLGN3 shedding, TSP-1 synaptogenesis and BDNF-TrkB potentiation are established laboratory findings, and recent experimental work already treats glutamatergic and receptor-tyrosine-kinase coupling together (Anastasaki 2025). The contribution is narrow and computational — to our knowledge the first spiking-network model coupling glioma growth to both an activity-dependent synaptic current and a diffusible paracrine field with use-dependent synaptic potentiation, making the reach and residual of each channel measurable — reported with its confounds stated plainly: results A/B/D are construction-determined; the 95% paracrine dominance and the apparent superiority of the secretion lever follow directly from the ~15% synaptic-fraction modelling choice and are not predictions of real drug efficacy — this model evaluates no drug; diffusion, clearance and secretion are order-of-magnitude values from generic brain extracellular-space parameters (Syková & Nicholson 2008), not measured NLGN3/TSP-1 kinetics; glioma units neither divide nor migrate; there is no vasculature, immune compartment, glutamate uptake, or inhibitory GABAergic neuron→glioma synapse; units are arbitrary with no external-data calibration. Scope-lock per Maya-Meta P2 (DOI 10.5281/zenodo.20621503): reproducible signatures within THIS architecture under THIS protocol — Property, not Law; a characterization of therapeutic reach in a two-channel model, NOT a clinical model of glioma. Perampanel, ADAM10-inhibitor and TrkB results in the literature are preclinical or in early trials and human survival benefit is unproven. Series: Part of the Maya-Vaidya Series — neuromorphic AI for clinical neuroscience. India-first. The Cancer sub-series arc: wire the tumour into the circuit (P7) → add the channel the circuit secretes (P8). 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