Audit fixed D18 credit and conditional MBON transfer (Phase 4AL)
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# Phase 4AL — credit specificity and conditional KC→MBON transfer
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## Purpose and frozen boundary
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This is a diagnostic audit of the already sealed Phase 4AK D18 branch, not
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conditioning, training, or a new learning candidate. Phase 4AK established its
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predeclared 100 ms KC representation gate; it did not establish appropriate
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credit assignment, functional associative memory, or biological fidelity of
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every omitted mechanism.
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Use all 120 Phase 4AK primary trials and all 24 exact-repeat trials. Keep the
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two cohorts and their two input modes separate. Repeats check reproducibility;
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they are not extra independent observations in the five-seed statistics. Do
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not replace seeds, select favorable odors, choose a best pair or compartment,
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or inspect old held-out dynamic outcomes to change this design.
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The inherited matched-energy mode matches expected input, not necessarily the
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realized event count of every stochastic trial; do not relabel it exact
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realized-count matching.
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All earlier raw, processed, frozen/reference, model and experiment artifacts
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remain read-only. Preserve the base CSR, anatomical counts, transmitter signs,
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LIF parameters, D18 operator, APL settings, eligibility-v2, and existing 14,232
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plastic-edge mask. All new records belong only to this new audit. No DAN
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stimulus is injected; no reinforcement is delivered to a brain; no learned
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`plastic_delta` is written. No decoder, action selection, game, RL, or visual
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interface is introduced.
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## Three distinct evidence levels
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1. **Exact baseline reconstruction.** Reconstruct target MBONs from the actual
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frozen full-network events using real edges, original arithmetic/order,
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initial states, arrivals, refractory acceptance, resets, and applicable APL
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handling. Require bitwise identity of events, per-neuron counts, and final
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V/g/ref against Phase 4AK D18. A failed or incomplete reconstruction blocks
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scientific interpretation of that replay; it is never rescued by plausible
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plots or by agreement of aggregate firing rates. Complete-audit integrity
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requires all 144 baseline replays; do not silently drop failed cases and
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report the remaining subset as the complete predeclared audit.
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2. **Virtual credit audit.** Replay the unchanged, existing float32 eligibility
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operator and inspect its state at the fixed tick-900 virtual gate, after
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that tick's original `mul → add → clamp` sequence. Tick-900 spikes are
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included. This is shadow accounting only, not dopamine delivery or weight
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updating; a before/after-update change is a different experiment. Do not
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treat virtual gate amplitude as measured dopamine concentration.
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3. **One fixed conditional sensitivity test.** Compare the exact baseline with
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one temporary replay applying uniform 25% depression to the whole existing
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plastic-edge mask. This uses the pre-existing maximum allowed fractional
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depression as a single declared diagnostic intervention. It is not a
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fraction scan, an eligibility-trained delta, a selected successful memory,
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or permission to enlarge the mask. The base weights remain unchanged; only
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the diagnostic effective amplitudes change, preserving edge identity and
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transmitter sign. On an independent incoming-weight copy, apply
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`weights[plastic] *= 0.75` throughout the full 100 ms replay, not only after
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tick 900. All presynaptic spike trains, including those of other MBONs and
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DANs, remain the original recorded trains. Do not save the overlay as a
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learned or official model.
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The 25% intervention is **not an upper bound on functional response**. LIF
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threshold, reset, refractory gating, and recurrent influences make responses
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nonlinear; the largest permitted fractional depression does not establish the
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largest attainable change in spikes, latency, or downstream activity.
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## Incoming-drive and overlap accounting
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Decompose actual MBON incoming drive into six mutually exclusive groups:
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- plastic KC→MBON;
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- non-plastic KC→MBON;
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- DAN;
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- MBON;
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- APL;
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- other.
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Use the frozen canonical IDs, mask membership and audited metadata, not guessed
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names or transmitter-to-cell-role substitutions. Preserve unknown role
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provenance inside the residual `other` group. Establish each edge's group once;
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do not reclassify it to improve the result. Report accepted/rejected arrivals,
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signed contributions, and roundoff/reset effects as the implementation makes
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available. The model's variable `g` is a model state; do not rename it a measured
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biophysical conductance or dopamine signal. A source's share of accepted drive
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is not its necessity, sufficiency, or unique causal contribution to a spike.
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Any ratio with a zero/undefined denominator must remain explicitly undefined.
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The sole set-similarity convention is empty/empty Jaccard = 1 with an explicit
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`empty_union` flag. Such pairs are counted separately and excluded from block
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overlap aggregates; this convention is never evidence of useful credit.
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For each cohort × mode, retain all 15 unordered pairs of its six odors: 60
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pair records in total. Report two separate three-of-five-seeds memberships for
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each odor: (1) a strictly positive frozen eligibility trace sampled after the
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tick-900 update, including tick-900 spikes, and (2) a strictly positive spike
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count anywhere in the full 100 ms trial. The primary virtual-credit grouping
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uses the first definition. The whole-window activity grouping is auxiliary;
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it cannot replace the primary grouping to rescue a result. These are
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descriptive reliability rules, not biological thresholds, top-K filters, or
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ways to delete cells/edges from replay. Preserve per-trial activity and
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eligibility alongside both aggregate memberships.
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Compute overlap on the actual A-active and B-active sets. In particular,
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`Jaccard(A_active, B_active)` must use their real intersection and union; never
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substitute the already disjoint sets `A_only` and `B_only`, whose zero
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intersection is true by construction. Shared, A-only, B-only, and inactive
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strata are useful descriptive partitions, not proof of stimulus-specific
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causation. Shared representations can support biological generalization;
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nonzero B effects are not automatically a defect, nor are they automatically
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evidence of valid generalization.
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Keep arithmetic/integrity checks separate from scientific results. Report all
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pairwise and trial-level outcomes without inventing an overall 120-trial
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biological PASS fraction, post hoc effect threshold, or pooled rescue gate.
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An absence of MBON spike change may coexist with a subthreshold change and
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does not mean the entire biological pathway is incapable of plasticity.
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## What a conditional replay can and cannot establish
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The baseline can establish that the saved events and the frozen operator
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reconstruct the saved MBON trajectory exactly. Virtual eligibility can reveal
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which real candidate edges would receive credit under that declared rule.
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The single depression replay can measure how the selected MBONs respond to
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that fixed intervention **with the external network event history held fixed**.
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It cannot establish closed-loop whole-brain necessity/sufficiency or learned
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behavior. If an MBON's replayed spikes change while its outgoing effects and
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the other neurons' events remain clamped to the old trial, MBON→DAN, MBON→MBON,
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and other feedback are not recomputed self-consistently. Their fixed incoming
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traces must not be described as counterfactual feedback responses. If the
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replay instead also clamps the target MBON's original reset/refractory gates,
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its result is narrower still: conditional drive/state accounting, not an
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independently recomputed functional spike response. State these scopes
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explicitly for each reported quantity.
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The anatomical D18 arrival delay is 18 × 0.1 ms = 1.8 ms. It is not the
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eligibility lifetime, a measured dopamine latency, or the CS–reinforcer
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association window. A 100 ms observation does not test memory retention,
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consolidation, extinction, reversal, or behavioral recall. Do not promote any
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successful replay to a dopamine-plasticity or learning candidate.
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## Primary evidence and non-measured assumptions
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- **Hige et al., Neuron (2015), DOI 10.1016/j.neuron.2015.11.003.** Pairing an
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odor with selected DAN activation produced odor-specific, compartment-local
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KC→MBON depression with order dependence. The reported induction did not
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require postsynaptic MBON spiking; overlapping KC representations predicted
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reduced specificity/generalization. This supports auditing the correct
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presynaptic and compartment credit, not requiring MBON spikes to define all
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plasticity. It does not specify MaleCNS per-edge learning parameters.
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[Author publication and paper](https://www.janelia.org/publication/heterosynaptic-plasticity-underlies-aversive-olfactory-learning-drosophila).
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- **Handler et al., Cell (2019), DOI 10.1016/j.cell.2019.05.040.** DopR1/DopR2
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pathways support opposing plasticity associated with different cue–DAN
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timing. This establishes why time ordering matters, not that the frozen
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float32 trace is a measured biochemical state or that one rule applies to
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every compartment. [Primary paper](https://www.sciencedirect.com/science/article/pii/S0092867419306117).
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- **Aso and Rubin, eLife (2016), DOI 10.7554/eLife.16135.** DAN cell types differ
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in memory formation, updating and persistence. PAM/PPL1 labels alone are
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not a license to assign a universal valence or a common temporal rule.
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[Primary paper](https://elifesciences.org/articles/16135).
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- **Aso et al., eLife (2014), DOI 10.7554/eLife.04580.** Different MBON types
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bias approach/avoidance, with combined activation supporting population
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integration. Assessing a population response is more appropriate than
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equating greater weight or total firing with positive memory. The current
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audit nevertheless has no behavioral decoder or demonstrated behavior.
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[Primary paper](https://elifesciences.org/articles/04580.pdf).
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- **Huang et al., Nature (2024), DOI 10.1038/s41586-024-07819-w.** Physiological
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measurements and a constrained model show heterogeneous, bidirectional
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PPL1 signaling and feedback interactions among memory units. This motivates
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explicit closed-loop limitations. Its fitted model weights and plasticity
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parameters are not MaleCNS anatomical counts or measurements to import into
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this frozen branch. [Primary paper](https://www.nature.com/articles/s41586-024-07819-w).
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- **Manoim et al., Current Biology (2022), DOI 10.1016/j.cub.2022.09.007, and
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Manoim Wolkovitz et al. (2026), DOI 10.1016/j.cub.2026.01.014.** KC lateral
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axonal mAChR-B modulation contributes to stimulus specificity; subsequent
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work identifies voltage-dependent modulation relevant to active versus
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inactive KCs. Sparse coding plus a timed reinforcer is therefore not, by
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itself, proof of appropriate credit. These studies do not prove that an
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omitted receptor mechanism caused any result in this fixed model, and do
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not authorize a sign, gain, threshold, or receptor-parameter change.
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[2022 paper](https://www.sciencedirect.com/science/article/pii/S0960982222014518);
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[2026 paper](https://www.sciencedirect.com/science/article/pii/S096098222600014X).
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The frozen eligibility operator, tick-900 virtual gate, three-of-five activity
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summary, 25% uniform diagnostic depression, clamped event history, and chosen
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observation window are engineering/model assumptions. None is relabelled as a
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MaleCNS single-cell or synaptic measurement by citing the papers above.
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## Deferred functional-memory controls — not executed here
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A later explicitly authorized learning experiment would need pre/post CS+
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and CS− responses, reciprocal cue assignment, independent evaluation seeds,
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and reinforcement-free probes with updates disabled. CS-only, DAN-only,
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unpaired/yoked, D(t)=0, and frozen/delta=0 conditions distinguish associative
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effects from exposure, transient state, adaptation and unrelated modulation.
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Real DAN-only stimulation is not universally expected to have zero effect;
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that prediction depends on the declared model and compartment. Retention
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requires its own observation interval, and any model-specific output effect
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must remain distinct from a behavioral-memory claim. No such controls are
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silently replaced by virtual credit or the 25% sensitivity test.
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Google/DeepMind's [FlyBody work](https://www.nature.com/articles/s41586-025-09029-4)
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provides body physics and artificial RL controllers, not evidence for this
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KC→MBON credit rule. Google's [MaleCNS author resource](https://research.google/blog/a-connectomics-milestone-mapping-the-complete-male-fruit-fly-brain/)
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supports the anatomical resource, not measured dopamine kinetics or successful
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learning in this model. Neither permits bypassing the present mechanism audit.
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