digital-drosophila/models/male-cns-lif/terminal-scope-diagnostic-v1/PROTOCOL.md

Phase 4AB — calyx contact-scope counterfactuals

This is an exploratory mechanism diagnostic, NOT an APL physiological model, learning experiment, parameter calibration or new formal runtime candidate. All previous scientific artifacts remain read-only. Only new output directories are permitted. No additional download is required.

Question and predeclared controls

Does removal of anatomically labelled calyx PN→KC input alter persistent KC activity without also removing the same PNs' antennal-lobe output?

Select PN/ROI pairs from actual Phase 4AA APL→ALPN synaptic contacts whose primary_post is exactly CA(L) or CA(R). Select PN→KC contacts only when their source PN and actual primary_post match that pair. This is ROI-level co-location, not proof of the same bouton, receptor, physiological coefficient, or even a per-presynaptic-site ROI annotation. primary_post labels the postsynaptic site. Never reclassify CentralBrain-unspecified by proximity.

Compare four conditions on the same eligible PN set:

1. Frozen reference; no changed weights or injected current.
2. Block only the matched CA PN→KC contact component.
3. Block all PN→KC output of those PNs, irrespective of ROI.
4. Block all fast outgoing synaptic weights of those PNs (broad scope control).

These are complete-block engineering interventions, not estimates of biological APL inhibition. There is no strength sweep or winner selection. Condition 4 does not silence PN somata or alter their force requests. The frozen graded APL input matrix remains active in all four conditions; condition 4 is therefore not a complete PN knockout. All fast edge slots remain present. Output masks are not plastic masks, and nothing is written back to base CSR or an old model.

For condition 2, the in-memory diagnostic effective weight is float32(float64(frozen_effective_weight) * (raw_count - CA_count) / raw_count). The linear per-contact decomposition is an engineering consequence of the existing linear weight model, not a measured transmitter-release law. At strength zero there is no arithmetic or write at all; identity must be exact. Conditions 3/4 set only the declared fast effective weights to zero. Anatomical counts, transmitter signs, LIF/refractory/delay, APL matrices and calibration, eligibility-v2 and the 14,232 plastic-edge mask remain frozen.

Trials and measurements, declared before results

Use all six old calibration odors, seed 131101, the frozen Phase 4V DoOR→PN request generator, 120 ms stimulus followed by observation to 1,000 ms. Do not consume held-out odors. Reset all states between trials. Repeat every condition for odor 0 to test exact determinism. No DAN reinforcement or weight training.

Record all spike events, all final counts/V/g, watched PN/KC/ALLN states, original force requests and their accepted/preexisting/blocked status, KC active fraction, late KC82312/VA6/ALLN activity (500–1,000 ms), and class-wise counts. All conditions share requested inputs; delivered events need not match because recurrent state and refractory periods can change. Explicitly report this distinction.

Unmodified trials must reproduce Phase 4Z whole events, watched states and Phase 4Y final arrays bit-for-bit. Each first-odor repeat must be exact. Run the five frozen Phase 4C trials against the deterministic-v2 archived oracle in new output paths. Original v1 files remain preserved, not relabelled as deterministic.

Additionally, replay the first frozen trial with its recorded events fixed, using the frozen ordered reduction and 18-step queue to validate locality: no terminal mask affects non-KC arrivals; broad controls may do so. This fixed-event test only measures the direct operator, not whole-brain causality.

Interpretation gate

Reduced KC activity alone is not repaired encoding or memory. A broad blockade can destroy useful drive. If CA blockade fails to remove the late KC response, report that it is insufficient under this model; do not increase gain or relabel unknown contacts. If it succeeds while ALPN/ALLN persist, report scope-specific model counterfactual evidence, not proof that biological APL has that strength. No result in this phase can generate a learned/physiological candidate.

Source boundaries

• MaleCNS official v1.0 syn-partners, CC BY 4.0, already verified in Phase 4AA: https://male-cns.janelia.org/download/
• Prisco et al. (2021), doi:10.7554/eLife.74172: local calyx APL interactions; does not assign MaleCNS edge-specific inhibition coefficients.
• Amin et al. (2020), doi:10.7554/eLife.56954: spatially localized APL activity and inhibition; does not validate the present engineering complete-block rule.

Unknown: bouton identity, receptor distribution, strength/time course of terminal release modulation, and whether adding such physiology would rescue memory. No game, decoder, RL, visual input, threshold/eta tuning, or next-phase training.