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# Tripartite Synapse — Biological Reference (companion to v16 pseudocode)
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> Companion to `tripartite_synapse_v16_pseudocode.md` · principle: `logic_principles_v3`.
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> v16 gives NIGHT a hierarchy of homeostatic actors at scales above the single synapse, and a
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> phased structure. The actors of consolidation are not the actors of transmission: by day the
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> six local components transmit; by night a hierarchy — astrocyte territory, the whole neuron,
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> and (as an external signal) the assembly/network — renormalizes and reallocates. Early-night
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> cycles downscale the day's transient changes (synaptic homeostasis); later cycles consolidate
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> the survivors. Occupancy filled by day (receptor surface, channel coupling) is returned to
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> baseline each night, so only what was written into a structural ceiling persists.
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---
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## The three synaptic components and their support structures
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A SYNAPSE is composed of three first-class components:
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- **PRE** — presynaptic bouton (the axon's terminal at this synapse)
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- **POST** — postsynaptic spine (the dendrite's terminal at this synapse)
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- **ASTRO** — astrosynapse, the perisynaptic astrocytic process (the astrocyte's terminal)
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Each has an upstream support structure that supplies it:
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- **AXON** supplies PRE (transmission + transport from soma)
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- **DEND** supplies POST (integration + transport from soma)
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- the **astrocyte cell body** supplies ASTRO (energy + ECM material)
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- **SOMA** is the integrating center and the root of neuronal material
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The compartment analogy: AXON:PRE = DEND:POST = astrocyte-body:ASTRO = supply line : terminal.
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---
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## Resource variables
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### DAY budget (one per component)
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Aggregates fast energy AND fast consumables — everything needed to run moment-to-moment.
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- **pre_budget** — ATP for VGCC gating, vesicle fusion (SNARE), VATPase vesicle refill,
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plus fast consumables: vesicle membrane lipids, synaptotagmin recycling.
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- **post_budget** — ATP for the NaK pump (membrane reset after current), NMDA current
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handling, plus fast actin monomers for transient spine changes and receptor-recycling lipids.
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- **dend_budget** — ATP for bAP propagation (NaK reset along branch), local translation
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(ribosome running cost), SERCA Ca²⁺ resequestration, plus fast mRNA consumed by translation.
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- **soma_budget** — ATP for AP generation (Na⁺/K⁺ currents + NaK reset), CREB
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phosphorylation, nuclear Ca²⁺ handling, plus shipping running costs.
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- **axon_budget** — ATP for AP propagation at nodes of Ranvier, kinesin/dynein motor
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running cost, fast myelin maintenance.
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- **astro_central_budget** — ATP from glycolysis at the astrocyte cell body; funds EAAT
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clearance, serine→D-serine synthesis, lactate export, fast process motility.
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### astro_lactate[i]
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Lactate exported from the astrocyte cell body to synapse i. Biologically: glucose →
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(glycolysis) → lactate, released into extracellular space, absorbed by neuronal MCT2
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transporters, converted to pyruvate → TCA → ATP in the neuron's mitochondria. The astrocyte
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is the primary fast-energy supplier to pre, post, and dend.
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### NIGHT energy (one per component) — NOT recoverable
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ATP for structural assembly. Distinct from DAY budget because it is spent on building, and
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the work of assembly is thermodynamically gone once done (cannot be recovered by disassembly).
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- pre_energy: RIM/Munc13 incorporation, VGCC clustering.
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- post_energy: CaMKII anchoring, actin polymerization, PSD scaffold remodeling.
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- dend_energy: mitochondria incorporation, cytoskeletal reinforcement.
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- soma_energy: ribosome biogenesis, ion-channel incorporation.
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- axon_energy: myelination, microtubule stabilization.
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- astro_energy: process retraction, ECM secretion, racemase upregulation.
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### NIGHT material (one per component) — RECOVERABLE
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Slow structural proteins. Recoverable because disassembly (LTD) returns the proteins to a
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reusable pool (ubiquitin-proteasome → amino acids; internalized receptors → endosomal reserve).
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- **soma_material** (root) — all neuronal structural proteins from CREB-driven synthesis:
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AMPA subunits, PSD scaffold, AZ scaffold, mRNA transcripts (Arc, BDNF), organelles.
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- **dend_material** — from soma: Arc/plasticity mRNA, mitochondria, cytoskeletal proteins,
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AMPA subunits in transit to spines.
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- **post_material** — from dend: AMPA receptor subunits (GluA1/2), PSD scaffold (PSD-95,
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SHANK, Homer), structural actin, CaMKII.
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- **axon_material** — from soma: kinesin/dynein motors, microtubule components, myelin proteins.
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- **pre_material** — from axon: RIM, Munc13, VGCC subunits, structural vesicle proteins.
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- **astro_material** (root: astrocyte cell body) — EAAT proteins, serine racemase, ECM
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proteins (Glypicans, Thrombospondins), process cytoskeleton.
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**Why energy and material are separate in NIGHT but combined in DAY:** during DAY both are
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fast consumables replenished on the same timescale, so one `budget` variable suffices. During
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NIGHT they diverge — material is recoverable after LTD, energy is not — so they must be two
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variables. This asymmetry (material returns to the pool, energy is gone) is what makes one
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synapse's depression genuinely fund another's potentiation.
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---
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## Structural variables (strength ceilings — written in NIGHT)
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Each aggregates several correlated structural properties into one capacity.
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- **pre_structure** — active zone capacity:
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slot_ceiling (number of vesicle docking slots) + VGCC_coupling (Ca²⁺-channel proximity to
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slots, sets release efficiency) + refill_ceiling (max RRP replenishment rate).
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- **post_structure** — spine sensitivity capacity:
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slot_ceiling (number of PSD anchoring slots for AMPA) + spine_volume (local reserve and
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actin machinery) + reserve_ceiling (endosomal AMPA pool size).
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- **dend_structure** — branch capacity:
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bAP_fidelity(position) (mitochondrial density sets propagation strength, attenuates with
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distance) + translation_ceiling (local mRNA capacity) + transport_speed (cytoskeletal integrity).
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- **soma_structure** — somatic output capacity:
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baseline_threshold (inverse: ion-channel density at axon initial segment) + AP_reliability
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(Na⁺ channel density) + synthesis_ceiling (ribosome density + CREB machinery).
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- **axon_structure** — axonal capacity:
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propagation reliability (myelination density) + transport_ceiling (motor density + microtubule
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integrity) + mitochondrial density.
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- **astro_structure** — astrosynaptic environmental capacity:
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perisynaptic_distance⁻¹ (wall proximity — closer = more glutamate contained) + EAAT_density
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(clearance ceiling) + Dserine_tonic (baseline co-agonist) + ECM_integrity.
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**Self-reinforcing both directions:** tighter wrap + more tonic D-serine make future
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potentiation easier; looser wrap + zero tonic D-serine make future depression easier.
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---
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## Budget ceilings (endurance ceilings — written in NIGHT)
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- **{component}_budget_ceiling** — the maximum fuel the component can hold / the maximum
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duration of sustained behavior. Biologically: mitochondrial density and local fuel-storage
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capacity. Built by activity-driven mitochondrial biogenesis; lost by mitophagy when idle.
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Parallel to structure: structure is strength capacity, budget_ceiling is endurance capacity.
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---
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## Trace variables
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### fast_trace (one per component) — DAY only, decays automatically
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The local record of recent activity that biases the next behavior.
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- **pre_fast_trace** — residual presynaptic Ca²⁺ after spikes (τ≈100ms). Biases NT release
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(facilitation) and provides tagging eligibility.
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- **post_fast_trace** — spine Ca²⁺ amplitude × rise-speed (τ≈tens ms). Encodes the LTP-vs-LTD
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instruction (fast rise → CaMKII → potentiation; slow rise → phosphatase → depression).
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- **dend_fast_trace** — branch Ca²⁺ from bAP + spine spillover (τ≈300ms). Integrates branch co-activity.
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- **soma_fast_trace** — nuclear Ca²⁺ from each AP (τ≈seconds). Drives toward CREB activation.
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- **axon_fast_trace** — propagation load (τ≈seconds). High load → Na⁺ inactivation at branch
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points → propagation failure (this is axonal short-term depression).
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- **astro_fast_trace** — perisynaptic Ca²⁺ from mGluR5 activation by glutamate spillover
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(τ≈seconds). Drives D-serine release.
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### soma timing traces (emergent refractory + adaptation + alignment)
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- **soma_Na_inactivation** (τ≈ms) — sodium-channel inactivation after an AP. Its recovery IS
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the refractory period (emergent, not a hardcoded timer). High → absolute refractory; decaying
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→ relative refractory; recovered → normal.
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- **soma_adaptation** (τ≈100s of ms) — slow K⁺ channel (SK/M-type) activation accumulating
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over a spike train, raising threshold. This is spike-frequency adaptation.
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- **soma_refractory_alignment** — deposited when a suprathreshold input arrives during
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refractoriness (a missed coincidence). Speeds future recovery so the soma aligns to its input
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rhythm. Bottom-up: no rhythm is represented; alignment emerges from accumulated local
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mismatches and decays when mismatches stop (self-limiting).
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### possible_tag (one per component) — intermediate, τ≈s–min
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Graded accumulation of tagging eligibility. For POST, this is the CANDIDATE tag lifetime.
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### endurance_need (one per component) — intermediate, τ≈s–min
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Deposited when budget depletion interrupts a behavior that was on a LOCALLY successful
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trajectory. Records that fuel — not structure, not significance — was the binding constraint
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on a forming success. Requires NO dopamine (homeostatic, not associative).
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**Local success proxy per component** (each uses only its own state + arrived signals):
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- PRE: own fast_trace high (was releasing strongly), optionally amplified by retrograde
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messenger (endocannabinoid / NO / BDNF) that has arrived.
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- POST: own Ca²⁺ climbing toward tagging threshold (naturally local).
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- DEND: own branch strongly active (high branch voltage/Ca²⁺) when propagation fell short.
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- SOMA: own nuclear Ca²⁺ climbing toward CREB.
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- AXON: own propagation load high (was carrying a strong train).
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- ASTRO: own local glutamate/Ca²⁺ high (was under heavy clearance/D-serine demand).
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### tag (one per component) — DAY→NIGHT bridge, τ≈hours
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The validated record of significance that survives to NIGHT and gates strength commits.
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Formed by coincidence of local eligibility + non-local validation (dopamine).
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**POST is special — two-phase, three coincidences:**
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- CANDIDATE: local Ca²⁺ above threshold + astrosynapse D-serine present (coincidence 1).
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- amplified when bAP confirms soma fired (coincidence 2).
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- STABLE: CANDIDATE + dopamine within stabilization window (coincidence 3).
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Biologically: early CaMKII creates a labile tag (early-LTP); PKA driven by dopamine via D1R
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stabilizes it (late-LTP). Without dopamine, the candidate degrades — early-LTP reverses.
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---
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## Behaviors — biological meaning
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### PRE | AP — neurotransmitter release
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`NT_flux = RRP × sat(pre_fast_trace, K_release)` models continuous NT release proportional to
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the readily-releasable pool and a saturating Ca²⁺ drive (synaptotagmin's cooperative Ca²⁺
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sensitivity, simplified to a saturating curve). RRP depletes as released (short-term depression
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as a consequence) and refills via VATPase (energy-throttled, so low budget deepens depression).
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The mGluR2/3 brake is presynaptic autoinhibition by spillover (Gi → reduced VGCC opening).
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### POST | NOT_bAP — three calcium sources, two plasticity cases
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- **Source 1 (AMPA):** glutamate opens AMPA → depolarizing current + small Ca²⁺; the
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depolarization begins ejecting the NMDA Mg²⁺ block.
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- **Source 2 (NMDA):** if depolarized enough (Mg²⁺ ejected) AND D-serine present (astrocyte
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co-agonist) AND glutamate bound → large Ca²⁺ influx. This is the coincidence detector.
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- **Source 3 (bAP, separate context):** back-propagating AP adds depolarization + Ca²⁺,
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amplifying an existing signal supralinearly.
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- **Case 1 (STP):** high Ca²⁺ drives AMPA receptors from the local reserve to the surface,
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bounded by the anchoring-slot ceiling. Fast, reversible, NO dopamine. When Ca²⁺ falls,
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receptors drift back — short-term depression as a passive consequence, never signaled.
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- **Case 2 (LTP tag):** high Ca²⁺ + (later) dopamine sets the tag that NIGHT uses to raise the
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slot ceiling. NIGHT builds slots; DAY fills them.
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### DEND | bAP — bidirectional signaling
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Propagates the bAP from soma toward spines (fidelity attenuates with distance — distal spines
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get weaker confirmation, are harder to potentiate) and integrates spine signals toward the soma.
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### SOMA | AP — integration, firing, emergent timing
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Fires when integrated branch input exceeds a threshold that is the baseline (from structure)
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raised by adaptation and modulated by neuromodulators, gated by the emergent refractory state.
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Each AP deposits three traces (inactivation → refractory, adaptation → threshold rise, nuclear
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Ca²⁺ → plasticity). The soma is the coincidence detector at the cellular scale (nuclear Ca²⁺ +
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dopamine → CREB), and the production bottleneck: its tag gates how much material all downstream
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components get in NIGHT.
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### AXON | AP — reliable propagation with frequency-dependent failure
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Propagation reliability is set by myelination and degraded by high-frequency load (Na⁺
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inactivation at branch points = axonal STD). The axon also transports material to boutons and
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sets the timescale of presynaptic structural commits.
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### ASTRO | CONTINUOUS — gatekeeper and energy hub
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Clears glutamate (EAAT), supplies D-serine (the NMDA co-agonist that gates postsynaptic LTP),
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and distributes lactate to the territory by demand-weighting (active synapses generating more
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clearance load pull more fuel; slow synapses get less). The same spillover that excites the
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astrocyte (mGluR5 → Ca²⁺ → D-serine) also brakes the presynapse (mGluR2/3 → Gi) — one signal,
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opposite effects via different receptors. The astrocyte is the energy root and the gain control
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of the whole synapse.
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---
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## NIGHT operations — biological meaning
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- **Step 1 (replenish/distribute):** overnight protein synthesis peaks (CREB-driven, gated by
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soma_tag — corresponds to slow-wave-sleep replay). Soma material flows to branches/axon then
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spines/boutons; astrocyte material flows to astrosynapses, tag-weighted.
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- **Step 2 (strength commits):** tagged components build structure — more slots, tighter
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coupling, tighter astrosynaptic wrap. Coherence bonus when pre+post+astro all tagged (the
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whole synapse agrees). astro_structure self-reinforces.
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- **Step 2b (endurance commits):** components with high endurance_need build budget_ceiling —
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mitochondrial biogenesis. Competes with step 2 for the same material/energy.
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- **Step 3 (passive decay):** both ceilings decay; maintenance from the remaining pool resists
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decay only where sufficient. Depotentiation and endurance-loss are both by neglect — no
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signal weakens anything; unmaintained capacity simply drifts down. Recovered material (not
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energy) returns to pools.
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- **Step 4 (homeostatic scaling):** if the soma fired too much overall, all synapses scale down
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proportionally (sleep-associated global downscaling), preserving relative differences.
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- **Step 5 (clear traces):** fast traces, possible tags, endurance needs, and soma timing traces
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reset; tags below expiry clear, above-expiry tags carry forward (multi-night consolidation);
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structure and budget_ceiling persist.
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### Shockwave lockdown
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Emergency global astrocytic Ca²⁺ wave → GABA + ATP release → mass AMPA internalization and
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hyperpolarization. Bypasses budget gates. A circuit breaker against runaway excitation.
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---
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## Pool-filling: private reserve vs contested supply
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The pseudocode uses two filling primitives, distinguished by where the resource comes from.
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**`fill` (private reserve).** The pool is replenished from a source the component owns
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outright, uncontested by siblings, bounded by the component's own ceiling and a rate cap.
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- RRP refill — vesicles mobilized from the bouton's own reserve pool toward the docking-slot
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ceiling, rate-limited by VATPase. The reserve is private to the bouton.
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- SOMA self-replenish — the soma fuels itself from its own mitochondria toward its budget
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ceiling. No other component draws on it.
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**`refill` (contested supply).** The pool is replenished from a supply that multiple
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components compete for, rationed by demand (gap to ceiling).
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- pre/post/dend/axon budgets — drawn from astrocytic lactate (shared across all synapses the
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astrocyte wraps) plus shipment from soma/axon/dendrite (shared across downstream targets).
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**Neither primitive (their own forms).** Some inflows are not fills toward a ceiling:
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- AMPA surface insertion — Ca²⁺-driven rate from the spine's private endosomal reserve, with
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an explicit passive drift-back (short-term depression) when Ca²⁺ is low. Not a steady fill.
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- D-serine release — demand-driven (saturating in astro Ca²⁺) and budget-limited, like NT
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release; a release process, not a pool top-up.
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- Root productions — `glycolysis(glucose)` at the astrocyte and `CREB_synth(soma_tag)` at the
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soma are the system's energy and material roots: raw inflows capped only by the external
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vascular supply, not fills toward an internal ceiling.
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The distinction matters biologically: a private reserve guarantees a component some autonomy
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(the bouton can refill its RRP from its own vesicles even when lactate is scarce), while a
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contested supply couples a component's fate to its neighbours' demands (operational budget
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fails first where many active synapses compete for the same lactate).
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---
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## PRE ↔ POST interaction: local computation, message-only coupling
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The presynapse and postsynapse never read each other's internal state. They interact only
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by writing to and reading from shared cleft channels. Each side computes entirely locally on
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what it has: its own variables plus whatever signals have arrived in the cleft. This is the
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message-passing realization of the locality principle.
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**Forward channel — glutamate (PRE → POST and ASTRO).** The presynapse writes glutamate via
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NT_flux. The postsynapse reads it (AMPA, NMDA) and the astrosynapse reads it (clearance,
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mGluR5). The astrosynapse clears it. PRE never knows whether POST responded — it only emits.
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**Gate channel — astro_Dserine (ASTRO → POST).** The astrosynapse writes D-serine; the
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postsynapse reads it as the obligatory NMDA co-agonist. POST cannot open NMDA without this
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arrived signal, but it does not read the astrocyte's state — only the delivered D-serine.
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**Backward channel + — retro_NO (POST → PRE).** When the postsynapse's NMDA opens (Mg²⁺
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ejected, D-serine present, glutamate bound), nNOS — physically tethered to the NMDA receptor
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through PSD-95 — synthesises nitric oxide (and, on a slower timescale, BDNF is released).
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These diffuse retrogradely to the presynapse. Biologically this is the classic retrograde
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messenger of LTP: it tells the bouton that its release landed on a postsynapse that genuinely
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responded. In the model, POST emits `retro_NO` proportional to its own NMDA-driven calcium —
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computed purely from POST's local state — and PRE reads it as `retro_NO_local`.
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`retro_NO_local` is exactly the grounding of the presynaptic endurance signal. The
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presynapse's local success proxy is "I was releasing strongly" (`pre_fast_trace` high). On
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its own that only says the bouton was working hard, not that the work mattered. `retro_NO`
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adds the missing confirmation — that the postsynapse responded — without PRE ever reading
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POST's calcium. So PRE deposits endurance need as `pre_fast_trace × (1 + retro_NO_local)`:
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strong release that was confirmed effective makes the strongest claim that fuel, not
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futility, was what interrupted a forming success. retro_NO is short-lived (NO degrades and
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diffuses within seconds), so the channel decays fast — confirmation must be recent to count.
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**Backward channel − — retro_eCB (POST → PRE).** When the postsynapse is strongly
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depolarised, it synthesises endocannabinoids (2-AG, anandamide) that diffuse retrogradely and
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bind presynaptic CB1 receptors, suppressing release. This is depolarisation-induced
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suppression of excitation (DSE) — a homeostatic negative feedback: an over-driven postsynapse
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tells the presynapse to release less. In the model, POST emits `retro_eCB` from its own
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membrane potential, and PRE reads it as `retro_eCB_local`, which reduces the release drive
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`sat(...) × (1 - retro_eCB_local)`. Again POST computes from its own state; PRE adjusts from
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the arrived signal; neither reads the other's interior.
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The two backward channels are opposite-signed messages the postsynapse sends about its own
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condition: retro_NO says "your input was effective — worth sustaining," retro_eCB says "I am
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saturated — ease off." Together with the forward glutamate and the D-serine gate, they make
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the synapse a fully message-coupled system of locally-computing components.
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**Why RRP refill is in NOT_AP only.** During an AP the bouton releases — RRP depletes. Refill
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(VATPase reloading vesicles from the reserve pool) is a recovery process that proceeds between
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spikes. Placing `fill(RRP, ...)` only in the NOT_AP context makes the AP context pure
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depletion and the NOT_AP context pure recovery. A consequence falls out for free: during
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sustained high-frequency firing there are many AP steps and few NOT_AP steps, so RRP depletes
|
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faster than it recovers — short-term depression deepens with frequency, with no explicit
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||||
depression rule. The release itself is throttled further when budget is low (VATPase refill
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||||
is energy-limited), coupling metabolic state to the depth of depression.
|
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||||
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||||
---
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## Presynaptic short-term potentiation — VGCC coupling occupancy
|
||||
|
||||
`VGCC_active` is the presynaptic parallel to the postsynaptic `AMPA_surface`. Both are MEDIUM-tier
|
||||
occupancy variables: a current operating value filled toward a NIGHT-built ceiling, no dopamine,
|
||||
reversible, drifting back when undriven.
|
||||
|
||||
Biologically, `VGCC_active` represents the effective coupling between voltage-gated calcium
|
||||
channels and the vesicle docking slots — how reliably each calcium influx is converted into
|
||||
release. Repeated eligible activity (accumulated `pre_possible_tag`) transiently tightens this
|
||||
coupling — through calcium-channel facilitation, active-zone protein phosphorylation, and
|
||||
channel-to-sensor proximity changes — raising release efficiency without changing the number of
|
||||
channels (which is the structural ceiling `pre_structure.VGCC_coupling`, written only at NIGHT).
|
||||
When eligibility falls, the coupling relaxes back to baseline over seconds-to-minutes: presynaptic
|
||||
short-term depression as the passive consequence of undriven coupling, never a signalled act.
|
||||
|
||||
This gives the presynapse a genuine intermediate-timescale memory it previously lacked — a
|
||||
"this bouton has been reliably active lately" state that outlasts individual spikes and bursts,
|
||||
filling the gap between the fast trace (residual calcium, ~100 ms) and the tag (hours). It also
|
||||
completes the capacity/occupancy symmetry across the synapse: both PRE and POST now fill a
|
||||
MEDIUM occupancy variable toward a PERSISTENT structural ceiling, rather than PRE reading its
|
||||
ceiling directly as if capacity and occupancy were the same thing.
|
||||
|
||||
|
||||
---
|
||||
|
||||
## NIGHT as iterated NREM cycles — the biology
|
||||
|
||||
The distributed, cyclic NIGHT models sleep-dependent consolidation more faithfully than a single
|
||||
commit step.
|
||||
|
||||
**Why cycles, not one event.** NREM sleep proceeds in repeated cycles (the ultradian ~90-minute
|
||||
rhythm, and within it the <1 Hz slow oscillation with its up- and down-states). Protein synthesis,
|
||||
hippocampal–cortical replay, and synaptic renormalization all advance incrementally across these
|
||||
cycles rather than in a single consolidation moment. Modeling NIGHT as a loop of cycles captures
|
||||
this: each cycle is a small, local round of produce → transport → incorporate.
|
||||
|
||||
**Production each cycle (the roots).** The soma's CREB-driven transcription/translation produces a
|
||||
batch of structural material per cycle, gated by the soma's own tag (replay-driven activity).
|
||||
The astrocyte cell body produces a batch of energy (glycolysis) and ECM material per cycle, capped
|
||||
by glucose. These are the two roots; everything downstream lives on what they ship.
|
||||
|
||||
**Transport over cycles (the descent).** Material and energy move one hop down the supply chains
|
||||
per cycle — soma → dendrite/axon → spine/bouton; astrocyte body → astrosynapses — by the same
|
||||
motor transport that carries cargo by day, now at the consolidation timescale. A distal bouton on
|
||||
a long axon therefore receives its material only after several cycles, so its consolidation lags
|
||||
a proximal one. This is the NIGHT-scale image of the transit delay.
|
||||
|
||||
**Incorporation and tag consumption (the commit).** A tagged synapse incorporates arrived material
|
||||
into structure (more receptor slots, tighter active zone, tighter astrocytic wrap) or into budget
|
||||
capacity (mitochondrial biogenesis), spending energy on the assembly. The tag is consumed in
|
||||
proportion to what was built — the molecular tag (CaMKII/PKA-maintained eligibility) is discharged
|
||||
as capture completes. A strong tag is satisfied early; a marginal one waits for later cycles.
|
||||
|
||||
**Two ways the night ends.** Either the standing tags are all spent (consolidation finished — the
|
||||
rested case) or the night's metabolic budget is exhausted (ran out of night — the overloaded
|
||||
case). Unspent tags are not discarded: they persist (decaying slowly) into the next day and
|
||||
compete again the next night, so importance is re-tested across nights and a marginal memory may
|
||||
consolidate over several nights or, if it decays first, never.
|
||||
|
||||
**Energy is the irreversible cost.** Material released when an unmaintained structure is pruned
|
||||
returns to the pool and is reused; the energy burned to build or to prune is gone. Across a
|
||||
lifetime this energy throughput bounds how much the system can ever consolidate — the metabolic
|
||||
arrow of time underlying the whole model.
|
||||
|
||||
|
||||
---
|
||||
|
||||
## NIGHT's hierarchy of actors — the biology
|
||||
|
||||
**Why the actors differ from DAY's.** Transmission is local — a bouton releases, a spine
|
||||
integrates, an astrosynapse clears. Consolidation is not: it involves quantities no single
|
||||
synapse can see. Whether one synapse's strengthening "fits" depends on the neuron's total
|
||||
synaptic weight; reallocating metabolic support depends on an astrocyte's whole territory;
|
||||
deciding which memories to replay depends on assemblies of neurons. So NIGHT is enacted by
|
||||
actors at higher scales, each conserving a quantity at its scale.
|
||||
|
||||
**The astrocyte territory (Tier 2).** The astrocyte cell body supports hundreds to thousands of
|
||||
synapses. By day it allocates lactate by demand; by night it reallocates its produced energy and
|
||||
ECM material across its whole territory, biased by the demand it accumulated and by replay. This
|
||||
is a genuine territory-level actor — the astrocyte is the metabolic arbiter of its domain, and
|
||||
its nightly reallocation decides which of its synapses can afford to consolidate.
|
||||
|
||||
**The neuron as a whole (Tier 1).** Synaptic homeostasis (the synaptic homeostasis hypothesis of
|
||||
Tononi and Cirelli) operates on the neuron's *total* synaptic weight: across sleep, the cell's
|
||||
synapses are renormalized downward multiplicatively, preserving relative differences while
|
||||
restoring overall excitability and freeing capacity. This is a neuron-scale operation — no synapse
|
||||
can perform it, because no synapse knows the cell's total weight. In the model the neuron
|
||||
accumulates that total by day and renormalizes it by night, scaling all the cell's structures by
|
||||
a common factor when the total exceeds the cell's budget.
|
||||
|
||||
**The assembly / network (Tier 0, external).** Systems consolidation — hippocampal–cortical replay
|
||||
— reactivates the day's patterns across ensembles of neurons during NREM, and this dialogue
|
||||
selects which assemblies are written into cortex. This is a network-scale process beyond a single
|
||||
neuron, so the model treats it as an external arrived signal (`replay_reweight`), exactly as it
|
||||
treats dopamine and glucose. Fully modeling it requires a network of these neurons.
|
||||
|
||||
**Occupancy downscaling — why only ceilings persist.** During the day, synapses fill occupancy:
|
||||
receptors trafficked to the surface (AMPA_surface), calcium-channel coupling tightened
|
||||
(VGCC_active), eligibility accumulated (possible_tag). These are transient and reversible. If they
|
||||
carried across the night undiminished, a synapse could become lastingly strong without ever
|
||||
earning a tag or paying the consolidation cost — bypassing the entire validation machinery.
|
||||
Multiplicative-global downscaling during early-night cycles returns occupancy to baseline. A
|
||||
synapse that was tagged and had its *ceiling* raised starts the next day strong; one that merely
|
||||
filled occupancy during the day starts back at baseline. The relative potentiation survives only
|
||||
where it was written into structure — which is precisely synaptic homeostasis enforcing that the
|
||||
slow tier carries the learning and the fast/medium tier is renewed each day.
|
||||
|
||||
**Why phased.** A single sweep cannot both reset and build, because building should act on the
|
||||
*post-reset* landscape. Early cycles are subtractive (downscale occupancy, renormalize weight,
|
||||
make metabolic room); later cycles are additive (commit the survivors). This is the NREM arc —
|
||||
slow-wave-dominated downscaling early, selective consolidation later — and it makes each cycle's
|
||||
*kind* depend on where in the night it falls, so the cycles are genuinely different operations,
|
||||
not installments of one.
|
||||
Reference in New Issue
Block a user