# Phase 4AC — upstream LIF semantics audit

Goal context: usable stimulus-specific associative learning remains unachieved.
This stage is a prerequisite diagnosis, never a substitute for that goal.

All raw, base CSR, old models/experiments and signs remain read-only. No eta,
threshold, gain, mask or APL calibration is changed. No conditioning, games,
decoder, visual stimulation, or new formal runtime is produced.

## New evidence and hypotheses

The official Shiu paper links philshiu/Drosophila_brain_model. Commit
91bdd1e7dcf193f3e7ca5a8933497fcef63b7960 (2024-09-14) model.py explicitly resets g
on a spike, declares both v and g `(unless refractory)`, uses linear integration
and strict `v > v_th`, and removes refractory time on Poisson-target neurons.
Current frozen Phase 4B/P instead retains g, decays/accepts arrivals during
refractory, uses explicit Euler, `>=`, and force requests respecting refractory.
The Phase 4B config documents its refractory-g policy, so this is a documented
adaptation difference, NOT evidence that deterministic CUDA regressed its oracle.
Neither implementation is automatically a more accurate MaleCNS physiology model.

## Scope of work allowed without replacing frozen brain dynamics

1. Preserve official code/license at a pinned commit, with hashes; do not execute
   downloaded code. Extract exact source statements into an evidence table.
2. Synthetic one-cell mathematical fixtures compare the frozen g policy with
   reset-only, refractory-only, and combined component ablations. Other arithmetic
   stays frozen. These are NOT a Brian2 reproduction (integration and scheduling
   also differ), and are not deployed to the MaleCNS brain.
3. Simulate only the UNCHANGED frozen dynamics on actual induced 2/3/5-neuron
   circuits selected from the already observed Phase 4Z path. One force request at
   t=0, then no input, for 1,000 ms. Include no-input and real-edge feedforward
   controls. Missing external network inhibition/feedback is explicitly excluded;
   a sustained isolated response is not proof of whole-brain necessity.
4. Validate every frozen CPU small-circuit event/state against the unchanged CUDA
   kernel, using exact float32 ordered accumulation and delay=18 steps.
5. Recheck the five archived deterministic reference trials and all old hashes.

All single-cell amplitudes derive from the complete unique contact-count set in
the selected real subgraph, plus a one-contact unit fixture. Do not choose a
successful amplitude after observing outcomes. Add a refractory-arrival fixture
at t=0/1/2/2.2/2.3 ms and a sustained-input-then-off fixture (100 ms then100 ms).
These describe operator consequences, not measured cell physiology or tuning.

The full learning gate still requires >=5 training seeds, independent evaluation,
A-vs-neutral-B specificity in MBON/downstream, appropriate controls, acquisition,
reversal, retention and delayed-reward tests. Existing transfer PASS is not that.

## Next-stage authorization boundary

Testing alternative semantics or measured local physiology on the full MaleCNS
network would be a NEW model experiment, not an exact runtime optimization.
User confirmation is requested separately. This stage does not silently execute
or promote that experiment, even if synthetic ablations reduce firing.

## Caveats to record

W_syn=0.275 is the original paper's free parameter selected on its feeding circuit,
not a universal measured MaleCNS contact efficacy. g reset by itself does not make
the model equivalent to the author's Brian2 implementation. Old reference PASS
means consistency with our old oracle, not matching the original author software.