Archive MaleCNS research sources, provenance, bibliography and immutable data inventory
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# Phase 4Z — mechanism interpretation
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Post-run descriptive analysis, not a new candidate gate. No tuning, learning, new stimulus or sign hypothesis.
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The earlier generic label PN feedback is refined below using actual ALLN cell identities. Do not assume the residual loop is KC→MBON→PN feedback merely because that pathway exists in the literature.
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## Watched identities
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| neuron_idx | body_id | class | type | metadata transmitter | raw ground_truth |
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|---:|---:|---|---|---|---|
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| 30 | 10039 | ALPN | VL2a_adPN | acetylcholine | acetylcholine |
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| 179 | 10198 | ALPN | VA7l_adPN | acetylcholine | acetylcholine |
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| 484 | 10522 | ALPN | VL2p_adPN | acetylcholine | acetylcholine |
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| 1197 | 11289 | ALLN | lLN1_bc | acetylcholine | acetylcholine |
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| 1381 | 11478 | ALLN | lLN1_bc | acetylcholine | acetylcholine |
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| 1511 | 11620 | ALLN | lLN1_bc | acetylcholine | acetylcholine |
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| 1644 | 11761 | ALPN | VP1d+VP4_l2PN1 | acetylcholine | None |
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| 6065 | 16610 | ALPN | VA7m_lPN | acetylcholine | acetylcholine |
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| 6842 | 17484 | ALPN | DC2_adPN | acetylcholine | acetylcholine |
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| 82312 | 109321 | Kenyon_Cell | KC | acetylcholine | None |
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| 133666 | 527577 | ALPN | VA6_adPN | acetylcholine | acetylcholine |
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## Representative first-late ancestry
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Odor 0 / seed 131101 / frozen reference. Ordered source spike → edge arrival → target spike (ms). These are ranked event-supported contributions; no unique predecessor assertion.
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| source idx/type | target idx/type | source time | arrival time | target time | contacts | effective weight |
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|---|---|---:|---:|---:|---:|---:|
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| 1381/lLN1_bc | 1511/lLN1_bc | 496.1 | 497.9 | 498.3 | 235 | 64.625000 |
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| 1511/lLN1_bc | 1381/lLN1_bc | 498.3 | 500.1 | 500.5 | 283 | 77.825005 |
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| 1381/lLN1_bc | 1197/lLN1_bc | 500.5 | 502.3 | 502.6 | 259 | 71.224998 |
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| 1197/lLN1_bc | 133666/VA6_adPN | 502.6 | 504.4 | 504.5 | 104 | 28.600000 |
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| 133666/VA6_adPN | 82312/KC | 504.5 | 506.3 | 506.4 | 43 | 11.825000 |
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## Dominant PN arrival contribution
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| trial | PN idx/type | positive arrival fraction |
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|---|---|---:|
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| 0-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.213% |
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| 0-131101-frozen_reference | 133666/VA6_adPN | 36.346% |
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| 1-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.353% |
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| 1-131101-frozen_reference | 133666/VA6_adPN | 36.346% |
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| 2-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.339% |
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| 2-131101-frozen_reference | 133666/VA6_adPN | 36.223% |
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| 3-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.243% |
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| 3-131101-frozen_reference | 133666/VA6_adPN | 36.162% |
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| 4-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.183% |
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| 4-131101-frozen_reference | 133666/VA6_adPN | 36.223% |
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| 5-131101-DPM_fast_current_off | 133666/VA6_adPN | 36.383% |
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| 5-131101-frozen_reference | 133666/VA6_adPN | 36.393% |
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Fractions are sums of positive synaptic arrivals, not percentages of causal responsibility. Negative input, recorded APL and membrane dynamics are retained in exact CPU replay.
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The preidentified 1381↔1511 event motif occurs in 7/12 first-late ancestry paths. Full temporal edges and alternative inputs are retained.
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Conditional omission results are in replay/results.parquet and REPORT.md. They retain other source events; loss of spikes there is not evidence that a whole-brain ablation would produce the same result.
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Critically, omitting ALLN arrivals to a watched ALLN does not silence it in conditional replay: recorded PN and other inputs can still sustain high firing. Thus the 1381↔1511 motif cannot be called the sole cause or an isolated autonomous oscillator.
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Removing the existing VA6_adPN→KC82312 edge in conditional replay eliminates target late firing; removing ALLN input to VA6_adPN also eliminates its late firing. These are two conditional links, not a demonstrated whole-brain necessity chain.
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## Late firing of preidentified ALLNs
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| neuron_idx | late rate range Hz | min/max ISI ms | fraction ISI = refractory, range |
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|---:|---:|---:|---:|
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| 1197 | 456–456 | 2.20/2.20 | 1.00000–1.00000 |
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| 1381 | 454–456 | 2.20/2.20 | 1.00000–1.00000 |
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| 1511 | 456–456 | 2.20/2.20 | 1.00000–1.00000 |
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This is a measured property of the mathematical model, not a validated biological firing rate. Window-boundary counting can put spikes/window slightly above 1/refractory. No new biological runaway threshold is inferred.
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## Frozen APL replacement target coverage
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The frozen implementation zeroes all 5845 APL fast outgoing edges and reintroduces graded inhibition only on KC targets. 1212 non-KC edges (13712 anatomical contacts) have no direct graded replacement in this implementation.
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This includes 7 edges / 247 anatomical contacts onto the seven watched PNs. Raw edges and counts remain intact. These edges were not removed by this audit.
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This is an implementation coverage gap relative to the anatomical graph, not evidence that restoring a whole-neuron negative current would be biologically correct. APL inhibition of PN boutons is spatial/terminal-specific and a point-neuron approximation may not capture it.
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Primary study: Prisco et al., eLife 10:e74172 (2021), https://pubmed.ncbi.nlm.nih.gov/34964714/ . It reports reciprocal APL inhibition targeting PN boutons and KC dendrites; it does not provide these MaleCNS edge-specific effective parameters.
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No frozen APL parameter, edge, sign or output target was modified. Functional necessity of this coverage gap remains untested.
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## What input matching means
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All six paired request schedules match. Status differs for 61 requests in total; actual output at requested times differs for 52 requests.
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An accepted→preexisting transition changes the accepted-new count without removing the output spike. A blocked transition can change actual delivery. Thus accepted-new totals alone are insufficient to describe input matching.
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The first differing request is state dependent; this is an endogenous response to an existing intervention, not evidence of different external RNG. No clamp, injected substitute events or refractory override was introduced.
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The earlier closed-loop intervention remains interpretable as a total system effect under matched requests. It is not an estimate of a direct DPM effect holding actual PN output trains fixed.
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## Literature boundary
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Excitatory local antennal-lobe circuits and reciprocal local-neuron/PN excitation have experimental support. They must not automatically be relabeled inhibitory because the model has persistent activity.
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Shang et al., Cell 2007: https://pubmed.ncbi.nlm.nih.gov/17289577/
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Huang et al., Neuron 2010, functional connectivity of excitatory local interneurons: https://doi.org/10.1016/j.neuron.2010.08.025
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These experiments do not validate uniform current weights, this MaleCNS individual, or its simulated persistent firing. No receptor, adaptation or electrical-synapse parameters are inferred or inserted.
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Next priority is independent assessment of local AL-loop dynamics and input-interface causal controls, not changing dopamine learning rate. No official model replacement is justified.
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