**Axon**: Axon does not contain specific behavior. We might add balancing of ATP within PRE later. Here we comprehend it as a “cable” transporting the AP from SOMA to Presynapse. It expands BEH-PRE which:
- the associations between BEH-PRE, BEH-POST e BEH-SYN is performed by the module that instantiate the Neurons and the Atrocytes, for example BEH-EXH or BEH-INH from winnertakeall.
**Presynapse:** We treat each presynapse as standalone. The vesicle reserve pool is a strictly private, local resource of each individual presynaptic bouton. What is shared between synapses on the same axon are signals (neuromodulators) and metabolic resources (energy), but not the synaptic vesicles themselves.
- **Ca2+**: Calcium Ion entering the Presynapse when VCGG open that influence NT release. Normally returns to ~0 between spikes; stays elevated when pumps fail. They are key to check the concentration, release vescicles and modulation
- **Rrp**: Readily Releasable Pool: The Readily Releasable Pool consists of the vesicles that are "docked" and "primed" at the active zone of the synapse.
-- Location: Directly touching the presynaptic membrane.
-- Function: These are the first to be released when an action potential arrives.
-- Characteristics: This pool is very small (usually only about 0.5% to 5% of total vesicles) and can be exhausted quickly during high-frequency firing, leading to "short-term depression" of the signal.
Ci sono 4 casi che dipendono da RRP, Ca2+ e NT. L'idea e' che la quantita' di RRP sia il driver principale. Gli NT liberati sono di piu' al crescere di RRP e Ca2+ e di meno al crescere di NT. Gli NT nella sinapsi fanno da moderazione alla ulteriore liberazione di NT, ma non bloccano mai totalmente. NT suppression only matters when everything else is already at maximum — which is exactly the biological purpose: it prevents runaway release during peak activity, not during moderate activity.
ATP cost of Na/K-ATPase recharge on each AP. The cost is per action potential. Here we charge it at every release of NT. This is the dominant ATP drain at high firing rates.
probabilmente sta dentro VGCC? Possiamo metterlo come un controllo su fullness di Ca2+ e cmq spiegare che e' un floor a questo comportamento di CDI
CDI is calcium-dependent inactivation of VGCCs. The inactivation happens because Ca²⁺ enters through the channel and binds to a calmodulin tethered to the channel's intracellular face, physically blocking it from reopening. This is a local, channel-specific event — it requires Ca²⁺ to be flowing through that channel right now, not residual Ca²⁺ drifting in the cytosol between spikes.
So the rise increment should only fire when V_pre == 1 (the spike window when channels are actually open and Ca²⁺ is entering). The recovery, by contrast, should run every millisecond unconditionally — CDI de-inactivation is a continuous process that proceeds whenever Ca²⁺ dissociates from calmodulin, which depends on the ambient Ca_micro level at all times.
Limita rilascio NT: Dipende dalla concentrazione alta di Ca2+ nella PRE. Driver Ca2+ > 0 between spikes CDI -> 1, effective_conductance -> 0.
```Gen
context: CDIConcentration
contained_by: BEH-PRE
in_context: NOT AP # prima volta NOT in un contesto
rf: ( active: 60x )
condition: (Ca2+ full)
out_context: IncreaseCDIFast
condition: (Ca2+ medium)
out_context: IncreaseCDIMedium
condition: (Ca2+ empty)
out_context: DecreaseCDI
```
#### CaTrace concentration
Serve a dare la velocita' al trasporto di vesicles da RP a RRP. Ha un decadimento proprio il che dice alla Presinapsi di accellerare se da poco c'e' stata una spike, altrimenti di andare piu' piano. So after one second of silence Tr_Ca has fallen to ~37% of its peak value, after two seconds to ~14%, after three seconds to ~5%. It asymptotes toward zero but never exactly reaches it. Between spikes, Ca2+ falls toward zero as the pumps clear it.
- **Open** — zero active brakes. mGluR alone never escapes this group because its ceiling is alpha_mGluR = 0.4, meaning even at full it only removes 40% of conductance, leaving 60% — still above the 85% threshold. So mGluR is irrelevant to the open/not-open boundary. Only CDI and eCB decide.
- **Reduced/partial** — exactly one meaningful brake active. Either CDI has started building (medium), or eCB has risen from sustained postsynaptic activity, but not both simultaneously. The system is aware something is happening but has not compounded yet. This is the normal operating range during moderate sustained firing.
- **Suppressed** — two brakes multiplying. The compounding is what defines this zone — no single variable alone produces it (except CDI approaching full). 0.5 × 0.5 = 0.25 remaining is where the synapse starts losing significant transmission efficacy. Biologically this is the pre-silence warning zone: CDI is building from residual Ca²⁺ while eCB is already engaged from postsynaptic activity.
- **Closed — CDI** = full is the only reliable hard rule. Because CDI can reach 1.0 and appears as (1 - CDI_factor) in the formula, it alone drives conductance to zero regardless of eCB and mGluR state. The three-brake overlap corner case (eCB=full + CDI=medium + mGluR=full) also reaches here, but in practice CDI reaching full is the primary biological mechanism.
