digital-drosophila/models/male-cns-lif/mb-credit-transfer-audit-v1/EVIDENCE.md

Phase 4AL — credit specificity and conditional KC→MBON transfer

Purpose and frozen boundary

This is a diagnostic audit of the already sealed Phase 4AK D18 branch, not conditioning, training, or a new learning candidate. Phase 4AK established its predeclared 100 ms KC representation gate; it did not establish appropriate credit assignment, functional associative memory, or biological fidelity of every omitted mechanism.

Use all 120 Phase 4AK primary trials and all 24 exact-repeat trials. Keep the two cohorts and their two input modes separate. Repeats check reproducibility; they are not extra independent observations in the five-seed statistics. Do not replace seeds, select favorable odors, choose a best pair or compartment, or inspect old held-out dynamic outcomes to change this design. The inherited matched-energy mode matches expected input, not necessarily the realized event count of every stochastic trial; do not relabel it exact realized-count matching.

All earlier raw, processed, frozen/reference, model and experiment artifacts remain read-only. Preserve the base CSR, anatomical counts, transmitter signs, LIF parameters, D18 operator, APL settings, eligibility-v2, and existing 14,232 plastic-edge mask. All new records belong only to this new audit. No DAN stimulus is injected; no reinforcement is delivered to a brain; no learned plastic_delta is written. No decoder, action selection, game, RL, or visual interface is introduced.

Three distinct evidence levels

1. Exact baseline reconstruction. Reconstruct target MBONs from the actual frozen full-network events using real edges, original arithmetic/order, initial states, arrivals, refractory acceptance, resets, and applicable APL handling. Require bitwise identity of events, per-neuron counts, and final V/g/ref against Phase 4AK D18. A failed or incomplete reconstruction blocks scientific interpretation of that replay; it is never rescued by plausible plots or by agreement of aggregate firing rates. Complete-audit integrity requires all 144 baseline replays; do not silently drop failed cases and report the remaining subset as the complete predeclared audit.
2. Virtual credit audit. Replay the unchanged, existing float32 eligibility operator and inspect its state at the fixed tick-900 virtual gate, after that tick's original mul → add → clamp sequence. Tick-900 spikes are included. This is shadow accounting only, not dopamine delivery or weight updating; a before/after-update change is a different experiment. Do not treat virtual gate amplitude as measured dopamine concentration.
3. One fixed conditional sensitivity test. Compare the exact baseline with one temporary replay applying uniform 25% depression to the whole existing plastic-edge mask. This uses the pre-existing maximum allowed fractional depression as a single declared diagnostic intervention. It is not a fraction scan, an eligibility-trained delta, a selected successful memory, or permission to enlarge the mask. The base weights remain unchanged; only the diagnostic effective amplitudes change, preserving edge identity and transmitter sign. On an independent incoming-weight copy, apply weights[plastic] *= 0.75 throughout the full 100 ms replay, not only after tick 900. All presynaptic spike trains, including those of other MBONs and DANs, remain the original recorded trains. Do not save the overlay as a learned or official model.

The 25% intervention is not an upper bound on functional response. LIF threshold, reset, refractory gating, and recurrent influences make responses nonlinear; the largest permitted fractional depression does not establish the largest attainable change in spikes, latency, or downstream activity.

Incoming-drive and overlap accounting

Decompose actual MBON incoming drive into six mutually exclusive groups:

• plastic KC→MBON;
• non-plastic KC→MBON;
• DAN;
• MBON;
• APL;
• other.

Use the frozen canonical IDs, mask membership and audited metadata, not guessed names or transmitter-to-cell-role substitutions. Preserve unknown role provenance inside the residual other group. Establish each edge's group once; do not reclassify it to improve the result. Report accepted/rejected arrivals, signed contributions, and roundoff/reset effects as the implementation makes available. The model's variable g is a model state; do not rename it a measured biophysical conductance or dopamine signal. A source's share of accepted drive is not its necessity, sufficiency, or unique causal contribution to a spike. Any ratio with a zero/undefined denominator must remain explicitly undefined. The sole set-similarity convention is empty/empty Jaccard = 1 with an explicit empty_union flag. Such pairs are counted separately and excluded from block overlap aggregates; this convention is never evidence of useful credit.

For each cohort × mode, retain all 15 unordered pairs of its six odors: 60 pair records in total. Report two separate three-of-five-seeds memberships for each odor: (1) a strictly positive frozen eligibility trace sampled after the tick-900 update, including tick-900 spikes, and (2) a strictly positive spike count anywhere in the full 100 ms trial. The primary virtual-credit grouping uses the first definition. The whole-window activity grouping is auxiliary; it cannot replace the primary grouping to rescue a result. These are descriptive reliability rules, not biological thresholds, top-K filters, or ways to delete cells/edges from replay. Preserve per-trial activity and eligibility alongside both aggregate memberships.

Compute overlap on the actual A-active and B-active sets. In particular, Jaccard(A_active, B_active) must use their real intersection and union; never substitute the already disjoint sets A_only and B_only, whose zero intersection is true by construction. Shared, A-only, B-only, and inactive strata are useful descriptive partitions, not proof of stimulus-specific causation. Shared representations can support biological generalization; nonzero B effects are not automatically a defect, nor are they automatically evidence of valid generalization.

Keep arithmetic/integrity checks separate from scientific results. Report all pairwise and trial-level outcomes without inventing an overall 120-trial biological PASS fraction, post hoc effect threshold, or pooled rescue gate. An absence of MBON spike change may coexist with a subthreshold change and does not mean the entire biological pathway is incapable of plasticity.

What a conditional replay can and cannot establish

The baseline can establish that the saved events and the frozen operator reconstruct the saved MBON trajectory exactly. Virtual eligibility can reveal which real candidate edges would receive credit under that declared rule. The single depression replay can measure how the selected MBONs respond to that fixed intervention with the external network event history held fixed.

It cannot establish closed-loop whole-brain necessity/sufficiency or learned behavior. If an MBON's replayed spikes change while its outgoing effects and the other neurons' events remain clamped to the old trial, MBON→DAN, MBON→MBON, and other feedback are not recomputed self-consistently. Their fixed incoming traces must not be described as counterfactual feedback responses. If the replay instead also clamps the target MBON's original reset/refractory gates, its result is narrower still: conditional drive/state accounting, not an independently recomputed functional spike response. State these scopes explicitly for each reported quantity.

The anatomical D18 arrival delay is 18 × 0.1 ms = 1.8 ms. It is not the eligibility lifetime, a measured dopamine latency, or the CS–reinforcer association window. A 100 ms observation does not test memory retention, consolidation, extinction, reversal, or behavioral recall. Do not promote any successful replay to a dopamine-plasticity or learning candidate.

Primary evidence and non-measured assumptions

• Hige et al., Neuron (2015), DOI 10.1016/j.neuron.2015.11.003. Pairing an odor with selected DAN activation produced odor-specific, compartment-local KC→MBON depression with order dependence. The reported induction did not require postsynaptic MBON spiking; overlapping KC representations predicted reduced specificity/generalization. This supports auditing the correct presynaptic and compartment credit, not requiring MBON spikes to define all plasticity. It does not specify MaleCNS per-edge learning parameters. Author publication and paper.
• Handler et al., Cell (2019), DOI 10.1016/j.cell.2019.05.040. DopR1/DopR2 pathways support opposing plasticity associated with different cue–DAN timing. This establishes why time ordering matters, not that the frozen float32 trace is a measured biochemical state or that one rule applies to every compartment. Primary paper.
• Aso and Rubin, eLife (2016), DOI 10.7554/eLife.16135. DAN cell types differ in memory formation, updating and persistence. PAM/PPL1 labels alone are not a license to assign a universal valence or a common temporal rule. Primary paper.
• Aso et al., eLife (2014), DOI 10.7554/eLife.04580. Different MBON types bias approach/avoidance, with combined activation supporting population integration. Assessing a population response is more appropriate than equating greater weight or total firing with positive memory. The current audit nevertheless has no behavioral decoder or demonstrated behavior. Primary paper.
• Huang et al., Nature (2024), DOI 10.1038/s41586-024-07819-w. Physiological measurements and a constrained model show heterogeneous, bidirectional PPL1 signaling and feedback interactions among memory units. This motivates explicit closed-loop limitations. Its fitted model weights and plasticity parameters are not MaleCNS anatomical counts or measurements to import into this frozen branch. Primary paper.
• Manoim et al., Current Biology (2022), DOI 10.1016/j.cub.2022.09.007, and Manoim Wolkovitz et al. (2026), DOI 10.1016/j.cub.2026.01.014. KC lateral axonal mAChR-B modulation contributes to stimulus specificity; subsequent work identifies voltage-dependent modulation relevant to active versus inactive KCs. Sparse coding plus a timed reinforcer is therefore not, by itself, proof of appropriate credit. These studies do not prove that an omitted receptor mechanism caused any result in this fixed model, and do not authorize a sign, gain, threshold, or receptor-parameter change. 2022 paper; 2026 paper.

The frozen eligibility operator, tick-900 virtual gate, three-of-five activity summary, 25% uniform diagnostic depression, clamped event history, and chosen observation window are engineering/model assumptions. None is relabelled as a MaleCNS single-cell or synaptic measurement by citing the papers above.

Deferred functional-memory controls — not executed here

A later explicitly authorized learning experiment would need pre/post CS+ and CS− responses, reciprocal cue assignment, independent evaluation seeds, and reinforcement-free probes with updates disabled. CS-only, DAN-only, unpaired/yoked, D(t)=0, and frozen/delta=0 conditions distinguish associative effects from exposure, transient state, adaptation and unrelated modulation. Real DAN-only stimulation is not universally expected to have zero effect; that prediction depends on the declared model and compartment. Retention requires its own observation interval, and any model-specific output effect must remain distinct from a behavioral-memory claim. No such controls are silently replaced by virtual credit or the 25% sensitivity test.

Google/DeepMind's FlyBody work provides body physics and artificial RL controllers, not evidence for this KC→MBON credit rule. Google's MaleCNS author resource supports the anatomical resource, not measured dopamine kinetics or successful learning in this model. Neither permits bypassing the present mechanism audit.