Digital Drosophila Archive
87 lines
4.8 KiB
Markdown
87 lines
4.8 KiB
Markdown
# Phase 4AB — calyx contact-scope counterfactuals
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This is an exploratory mechanism diagnostic, NOT an APL physiological model,
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learning experiment, parameter calibration or new formal runtime candidate.
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All previous scientific artifacts remain read-only. Only new output directories
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are permitted. No additional download is required.
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## Question and predeclared controls
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Does removal of anatomically labelled calyx PN→KC input alter persistent KC
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activity without also removing the same PNs' antennal-lobe output?
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Select PN/ROI pairs from actual Phase 4AA APL→ALPN synaptic contacts whose
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`primary_post` is exactly `CA(L)` or `CA(R)`. Select PN→KC contacts only when
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their source PN and actual `primary_post` match that pair. This is **ROI-level
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co-location**, not proof of the same bouton, receptor, physiological coefficient,
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or even a per-presynaptic-site ROI annotation. `primary_post` labels the
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postsynaptic site. Never reclassify `CentralBrain-unspecified` by proximity.
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Compare four conditions on the same eligible PN set:
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1. Frozen reference; no changed weights or injected current.
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2. Block only the matched CA PN→KC contact component.
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3. Block all PN→KC output of those PNs, irrespective of ROI.
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4. Block all fast outgoing synaptic weights of those PNs (broad scope control).
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These are complete-block engineering interventions, not estimates of biological
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APL inhibition. There is no strength sweep or winner selection. Condition 4
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does **not** silence PN somata or alter their force requests. The frozen graded
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APL input matrix remains active in all four conditions; condition 4 is therefore
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not a complete PN knockout. All fast edge slots remain present. Output masks are
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not plastic masks, and nothing is written back to base CSR or an old model.
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For condition 2, the in-memory diagnostic effective weight is
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`float32(float64(frozen_effective_weight) * (raw_count - CA_count) / raw_count)`.
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The linear per-contact decomposition is an engineering consequence of the
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existing linear weight model, not a measured transmitter-release law.
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At strength zero there is no arithmetic or write at all; identity must be exact.
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Conditions 3/4 set only the declared fast effective weights to zero. Anatomical
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counts, transmitter signs, LIF/refractory/delay, APL matrices and calibration,
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eligibility-v2 and the 14,232 plastic-edge mask remain frozen.
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## Trials and measurements, declared before results
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Use all six old calibration odors, seed 131101, the frozen Phase 4V DoOR→PN
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request generator, 120 ms stimulus followed by observation to 1,000 ms. Do not
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consume held-out odors. Reset all states between trials. Repeat every condition
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for odor 0 to test exact determinism. No DAN reinforcement or weight training.
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Record all spike events, all final counts/V/g, watched PN/KC/ALLN states, original
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force requests and their accepted/preexisting/blocked status, KC active fraction,
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late KC82312/VA6/ALLN activity (500–1,000 ms), and class-wise counts. All conditions
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share requested inputs; delivered events need not match because recurrent state
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and refractory periods can change. Explicitly report this distinction.
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Unmodified trials must reproduce Phase 4Z whole events, watched states and
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Phase 4Y final arrays bit-for-bit. Each first-odor repeat must be exact. Run the
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five frozen Phase 4C trials against the deterministic-v2 archived oracle in new
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output paths. Original v1 files remain preserved, not relabelled as deterministic.
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Additionally, replay the first frozen trial with its recorded events fixed, using
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the frozen ordered reduction and 18-step queue to validate locality: no terminal
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mask affects non-KC arrivals; broad controls may do so. This fixed-event test
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only measures the direct operator, not whole-brain causality.
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## Interpretation gate
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Reduced KC activity alone is not repaired encoding or memory. A broad blockade
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can destroy useful drive. If CA blockade fails to remove the late KC response,
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report that it is insufficient under this model; do not increase gain or relabel
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unknown contacts. If it succeeds while ALPN/ALLN persist, report scope-specific
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model counterfactual evidence, not proof that biological APL has that strength.
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No result in this phase can generate a learned/physiological candidate.
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## Source boundaries
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- MaleCNS official v1.0 syn-partners, CC BY 4.0, already verified in Phase 4AA:
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https://male-cns.janelia.org/download/
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- Prisco et al. (2021), doi:10.7554/eLife.74172: local calyx APL interactions;
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does not assign MaleCNS edge-specific inhibition coefficients.
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- Amin et al. (2020), doi:10.7554/eLife.56954: spatially localized APL activity
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and inhibition; does not validate the present engineering complete-block rule.
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Unknown: bouton identity, receptor distribution, strength/time course of terminal
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release modulation, and whether adding such physiology would rescue memory.
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No game, decoder, RL, visual input, threshold/eta tuning, or next-phase training.
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