The plasticity layer — consolidation and the reversible→chronified switch

The plasticity layer the structural atlas never had: a phase-correlation Hebbian update of the ephaptic kernel makes consolidation and after-effects representable, resolves the open continuous-versus-periodic dosing question (spaced leaves a larger retained trace, so the cap repairs and pacing beats holding), and builds the reversible-to-chronified switch later mood disorders need. With plasticity off it reproduces the frozen engine bit-for-bit. efficacy=0.

Every module so far read a static operating point: the frozen engine has no variable that changes with use. That gap is why the θ-cap chapters could show the cap paces the network but could not ask whether holding it there repairs anything — the substrate had nothing to retain — and why the cap's plasticity sign was left open [O]. This chapter adds the missing layer on top of the READ-ONLY engine: a slow phase-correlation Hebbian update of the ephaptic kernel W, W_ij ← max(0, W_ij(1+ηC_ij)) with C_ij = <cos(θ_j−θ_i)>. The rule form is forced [F] (standard phase-STDP, no free constant, row-stochastic so the ephaptic locality is preserved); the rate η is [O] and every sign below survives an η sweep (anti-tuning). Four results: consolidation and after-effects become representable; the open continuous-vs-periodic dosing question is resolved (spaced leaves a larger retained trace than massed — the cap repairs, and pacing beats holding); the reversible→chronified switch is built; and with η=0 the layer reproduces the frozen M9 coordination anchor bit-for-bit (a pure add-on). The layer, not an application: the mood and cycle disorders that use it are owed to later modules. efficacy = 0.

plasticity = the consolidation layer; the reversible→chronified switch the static atlas never had = a phase-correlation Hebbian update of the ephaptic W makes consolidation representable, resolves the open dosing question (spaced > massed), and turns a reversible excursion into a chronified one — the frozen engine has NO plasticity variable — which is why the θ-cap (§20-21) could only PACE, not repair, and why its plasticity sign was OPEN [O]. This layer adds a slow phase-correlation Hebbian update to the ephaptic kernel, W_ij ← max(0, W_ij(1+η·C_ij)) with C_ij = <cos(θ_j−θ_i)>, row-renormalised. The rule FORM is forced [F] (standard phase-STDP, no free constant, row-stochastic so the ~1/r³ ephaptic locality is preserved); the RATE η is [O] and every sign holds over an η sweep (anti-tuning), and the coupling-vs-bias map is the SAME k=κ/(1−|b|)[excit]/κ/(1+|b|)[inhib] cap 2κ as the SZ/epilepsy modules — no new tuned constant. Four results: (E0.1) driving the healthy point under plasticity then removing the drive leaves R at or above baseline (0.390→0.391) — consolidation / after-effects, over an η sweep; (E0.2) the same total cap dose delivered SPACED (periodic) leaves a LARGER retained structural trace ‖ΔW‖ than MASSED (continuous) (0.225 vs 0.115) — a spacing effect from pure phase-plasticity, so with plasticity the cap REPAIRS and pacing beats holding (resolving the §20-21 [O]); (E0.3) without plasticity (η=0) a faulted excursion fully REVERTS when the bias is removed (the §20 'paces not repairs / no rebound' result, now shown to be a consequence of the plasticity-free substrate), while with plasticity (η>0) it leaves a retained trace (0.394>0.390) — plasticity is the reversible→chronified switch (Axis-A firewall: a mechanism boundary, not a claim about the felt quality of chronic illness; consciousness_claim=0); (E0.4) η=0 reproduces the frozen M9 anchor R=0.38961455156044245 bit-for-bit and leaves W identical — a pure add-on (engine e61083ae…, tree 0fbf4988…, byte-unchanged). E0 is the LAYER, not a disorder; depression (T1b), bipolar (T2b) and addiction (T3a) import its substrate and are owed to later modules. efficacy=0; not medical advice; hard problem OPEN. [V mech]. this chapter

epilepsy = the over-synchronisation pole; the ictal state = collapse of the selective gate = excitatory bias drives R to the over-sync ceiling and all assemblies ignite; an anticonvulsant reverses it and raises the threshold — epilepsy is the over-synchronisation pole of the engine's synchrony axis (the global Kuramoto order parameter R on the measured ephaptic kernel, plus the M3 R19 ignition gate). An excitatory/disinhibitory E/I bias raises R monotonically toward the over-sync ceiling (0.422 > health 0.390); past a critical bias (+0.3) the selective single-winner gate collapses and EVERY candidate assembly ignites — the ictal state, a loss of GATING (Axis-A firewall: a mechanism boundary, not a claim about ictal experience; consciousness_claim=0). On one axis: autism-T (under-ignited) < health (selective) < schizophrenia (aberrant, some irrelevant) < epilepsy (all ignited). An inhibitory / threshold-raising anticonvulsant-class push moves R back down and restores the gate — it raises the seizure threshold by moving the operating point away from the over-sync ceiling (the same ceiling the θ-cap must stay below, §20). The static susceptibility is characterised; the ictal time-course is OWED to a state-switching layer (E2). efficacy=0; not medical advice. [V mech]. canonical §25

The layer the structural atlas never had

Autism on the T/O/W axes, schizophrenia at the over-ignition pole, epilepsy at the over-synchronisation ceiling — every result in the atlas so far has been read off a static operating point. Move a bias, the order parameter moves; remove it, the network returns. Nothing in the frozen engine changes with use, because the engine has no plasticity variable at all. That is not a small omission. It is precisely why the θ-cap operating-principle chapter could establish that the cap paces the network — across ON/OFF cycling there was no rebound and no acquired dependence — but could not say whether parking the network at the cap repairs anything, because the substrate had nothing in which to keep a change. The plasticity sign of the operating principle was left explicitly [O] for that reason. This chapter supplies the missing variable, and in doing so closes that open question.

The rule: Hebb read on phase (form forced, rate open)

On phase oscillators the time-averaged spike-timing plasticity window between two units reduces to a function of their phase difference: pairs that run in phase potentiate, pairs in anti-phase depress. It is Hebb's rule — fire together, wire together — read on phase. We take the steady-state pairwise phase correlation C_ij = <cos(θ_j−θ_i)> as the Hebbian signal and update the ephaptic kernel multiplicatively, W_ij ← max(0, W_ij(1+ηC_ij)), then row-renormalise. The form has no free constant: the diagonal stays zero, weights stay non-negative, and the row-renormalisation keeps the rows stochastic so the ~1/r³ ephaptic locality of the frozen kernel is preserved. The single rate η is [O] — representative, exactly as the absolute Hz, the ring geometry and R_BRAIN are [O] in M9 — and, crucially, the signs asserted below are required to hold over a sweep of η, so no number is fit to a target. The map from a drive or a faulted bias to an effective coupling is the same k = κ/(1−|b|) (excitatory) / κ/(1+|b|) (inhibitory), capped at 2κ, used in the schizophrenia and epilepsy modules. No new tuned constant enters.

Consolidation: the network remembers (E0.1)

The first thing the layer makes possible is the most basic, and the one the static engine simply could not express. Drive the network at the healthy operating point under plasticity, then switch the drive off and read the order parameter. It does not fall back to where it started: it sits at or above baseline (R 0.390 → 0.391, ΔR > 0), and the sign stays positive across the whole η sweep. The coordination has been written into the structure — a stimulation after-effect. This is the substrate for learning, for use-dependent change, for the lasting trace of an intervention: none of which a plasticity-free engine could represent, all of which fall out of one forced rule.

The dosing question, resolved: pace, don’t hold (E0.2)

The θ-cap chapters left a concrete device question open. If a cap-class stimulation has a fixed total budget, is it better delivered continuously (held at the cap) or in spaced bursts? With no plasticity the question is empty — nothing is retained either way. With the layer present it has an answer. Deliver the same total time-at-cap two ways: massed (one continuous run) and spaced (periodic ON/OFF bursts, the plasticity rule running through the OFF gaps). The spaced protocol leaves a larger retained structural trace per unit dose (∥ΔW∥ 0.225 vs 0.115 for massed) — a spacing effect emerging from pure phase-plasticity, the same direction learning science calls distributed practice. Two consequences follow, both sign-only. First, with plasticity present the cap repairs: it leaves a lasting trace, which is exactly the [O] the θ-cap operating principle could not resolve. Second, pacing beats holding — pulse, do not hold. The sign holds at every point of an η×epochs sweep. It is a direction that would change a protocol, not a dose and not an efficacy: efficacy = 0.

The reversible→chronified switch (E0.3)

The most consequential result is the cleanest. Drive a sustained faulted (excitatory) bias and then remove it. Without plasticity (η=0) the excursion fully reverts: the order parameter returns exactly to baseline. That is, precisely, the chapter-20 result — paces, not repairs; no rebound, no acquired dependence — now shown to be a consequence of the plasticity-free substrate, not a property of the cap. With plasticity (η>0) the same excursion leaves a retained trace that does not revert when the bias is removed (R holds at 0.394 > 0.390): a faulted state has written itself into the structure. Plasticity is the switch between a reversible state and a chronified one. It must be said exactly what this is and is not: a retained structural trace is a mechanism boundary, not a claim about the felt quality of chronic illness (Axis-A firewall — consciousness_claim = 0; the hard problem of experience stays open). The model speaks to whether a state can persist in the structure, not to what, if anything, that persistence feels like.

A pure add-on, and what it unlocks (E0.4)

The guard makes the discipline operational. With η=0 the layer reproduces the frozen M9 coordination anchor bit-for-bit (R = 0.38961455156044245) and leaves W identical to the kernel. Turning plasticity off recovers the frozen engine exactly: the engine file stays e61083ae…, the emergence tree stays 0fbf4988…, byte-unchanged. E0 adds; it does not alter.

And it is a layer, not a disorder. Its purpose is to be the foundation the temporal conditions stand on. Depression as the chronification of a low-coordination operating point, bipolar as the accumulation of episodes, addiction as sensitisation — each needs a substrate in which a state can write itself in and stay. E0 supplies that substrate once, as a reusable object; the mood and cycle modules that follow import it rather than re-deriving it. Everything here is an in-silico coupling state, not a clinical measure. This is a mechanism-level result about plasticity as represented in the VP framework — not medical advice, not a diagnosis, not a treatment protocol, and not a cure. efficacy = 0; the hard problem stays open.