iniziato ad aggiungere i behaviors attesi

neuron/BEH-AXO.md

@@ -25,43 +25,56 @@ container: BEH-AXO
 
 **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.
 
-**Behaviors** Related to:
+**Actors**:
 
 - Voltage (V_pre / membrane state)
--- Voltage increase from AP (external spike drive — V_pre = 1)
+  \-- Voltage increase from AP (external spike drive — V_pre = 1)
--- Voltage decrease from Na/K-ATPase recharge after each AP (we might need to include in the model)
+  \-- Voltage decrease from Na/K-ATPase recharge after each AP (we might need to include in the model)
-
 - NT (neurotransmitter / vesicle pools)
--- NT released from RRP (instead of modeling this as stochastic_release: p = p_release_base *Ca_micro, I'd like to model this as a function of Ca-micro, number of vescicles in RRP, modulated down by NT already released)
+  \-- NT released from RRP
--- NT replenishment in RRP from RP: (map_trace_to_speed: rate gated by Tr_Ca trace; fast when Tr_Ca > T_high, slow when Tr_Ca < T_low — the Ca2+ trace is the recruitment memory)
+  \-- NT replenishment in RRP from RP: (map_trace_to_speed: rate gated by Tr_Ca trace; fast when Tr_Ca > T_high, slow when Tr_Ca < T_low — the Ca2+ trace is the recruitment memory)
--- NT replenishment in RP from Astrocyte: (glutamine shuttle: refill_RP = Glutamine_pool * conversion_efficiency, runs once per minute; gated by ATP_level via conversion_efficiency)
+  \-- NT replenishment in RP from Astrocyte: (glutamine shuttle: refill_RP = Glutamine_pool *conversion_efficiency, runs once per minute; gated by ATP_level via conversion_efficiency)
   -- NT degradation / dilution from cleft: (passive: NT_cleft*= 1 - dt/tau_NT_decay each ms)
   -- NT clearance from cleft by Astrocyte EAATs: (cleared_NT = NT_cleft * 0.3, once per second)
-
 - VGCC (voltage-gated calcium channels)
--- VGCC increase in number by slow activity-dependent upregulation
+  \-- VGCC increase in number by slow activity-dependent upregulation
--- VGCC conductance suppressed by eCB (retrograde brake)
+  \-- VGCC conductance suppressed by eCB (retrograde brake)
--- VGCC conductance suppressed by mGluR autoreceptor tracks NT_cleft directly via Michaelis-Menten occupancy, fastest of the three brakes — no postsynaptic relay needed
+  \-- VGCC conductance suppressed by mGluR autoreceptor tracks NT_cleft directly via Michaelis-Menten occupancy, fastest of the three brakes — no postsynaptic relay needed
--- VGCC conductance suppressed by CDI (calcium-dependent inactivation) CDI rises with Ca_micro via k_CDI_rise, recovers only when Ca_micro falls — the metabolic silence lock
+  \-- VGCC conductance suppressed by CDI (calcium-dependent inactivation) CDI rises with Ca_micro via k_CDI_rise, recovers only when Ca_micro falls — the metabolic silence lock
-
 - Ca2+
--- Ca2+ intake via VGCC on each AP: only the fraction not captured by buffer enters Ca_micro
+  \-- Ca2+ intake via VGCC on each AP: only the fraction not captured by buffer enters Ca_micro
--- Ca2+ buffered into calbindin / calmodulin (fast, on spike): buffer saturates during sustained bursting: B_free -> 0
+  \-- Ca2+ buffered into calbindin / calmodulin (fast, on spike): buffer saturates during sustained bursting: B_free -> 0
--- Ca2+ released back from buffer into cytosol (slow recharge)sustains Ca_micro elevation under pump failure
+  \-- Ca2+ released back from buffer into cytosol (slow recharge)sustains Ca_micro elevation under pump failure
--- Ca2+ extruded by PMCA — primary pump, ATP-dependent: first to fail when ATP drops; largest ATP-dependent clearance term
+  \-- Ca2+ extruded by PMCA — primary pump, ATP-dependent: first to fail when ATP drops; largest ATP-dependent clearance term
--- Ca2+ extruded by NCX — fast exchanger, NOT ATP-dependent: floor mechanism: keeps clearing during metabolic failure; enables auto-reset when high-frequency drive stops 
+  \-- Ca2+ extruded by NCX — fast exchanger, NOT ATP-dependent: floor mechanism: keeps clearing during metabolic failure; enables auto-reset when high-frequency drive stops
--- Ca2+ pumped into ER by SERCA — slowest pump, ATP-dependent: also loads Ca_ER store; fails alongside PMCA under low ATP
+- Ca2+ pumped into ER by SERCA
--- Ca2+ stored in ER (Ca_ER) (Ca_ER += cleared_SERCA; ER store is a future IP3-release target)
+  \-- Active transport, ATP-dependent, slowest of the three pumps Clears Ca2+ from the cytosol (reduces Ca_micro). Loads the Ca_ER store as a byproduct.
-
+- Ca2+ stored in ER (Ca_ER). Passive reservoir. Fills gradually during normal activity via SERCA. Can be released back into the cytosol via IP3R channels when astrocyte IP3 signalling crosses threshold (not yet implemented — Ca_ER currently only increases). This release pathway would create a slow secondary Ca2+ surge independent of VGCC activity — relevant for plasticity and for amplifying the metabolic silencing cascade if added later.
 - CDI (calcium-dependent inactivation of VGCCs)
--- CDI rises with Ca_micro each ms: accumulates across inter-spike intervals under pump failure
+  \-- CDI rises with Ca_micro each ms: accumulates across inter-spike intervals under pump failure
--- CDI recovers when Ca_micro is low: rate -> 0 when Ca_micro is high — the self-locking feedback of CASCADE 5
+  \-- CDI recovers when Ca_micro is low: rate -> 0 when Ca_micro is high — the self-locking feedback
-
 - ATP
--- ATP decrease by PMCA / SERCA pumping: (each ms of Ca2+ clearance consumes ATP; modelled implicitly via the demand that sustains Glucose_level depletion in Loop 3)
+  \-- ATP decrease by PMCA / SERCA pumping: (each ms of Ca2+ clearance consumes ATP; modelled implicitly via the demand that sustains Glucose_level depletion)
--- ATP decrease by vesicle re-docking (RP -> RRP recruitment): (each refill_amount of vesicles moved to RRP costs ATP for priming/docking machinery; modelled implicitly in CASCADE 2 demand)
+  \-- ATP decrease by vesicle re-docking (RP -> RRP recruitment): (each refill_amount of vesicles moved to RRP costs ATP for priming/docking machinery)
--- ATP decrease by Na/K-ATPase recharge after each AP (largest single ATP cost per spike; drives CASCADE 2 during high firing)
+  \-- ATP decrease by Na/K-ATPase recharge after each AP (largest single ATP cost per spike)
--- ATP increase from Astrocyte metabolic support: glucose delivery is the root input — set Glucose_level < 1.0 to engage the full metabolic silencing cascade
+  \-- ATP increase from Astrocyte metabolic support: glucose delivery is the root input — set Glucose_level < 1.0 to engage the full metabolic silencing cascade
+
+**Behaviors**:
+
+- NT release
+  \-- NT_RRP (NT in vesicles in RRP) Piu' vicino alla fullness piu' release
+  \-- CaMicro (free calcium) Piu vicino alla fullness, piu' release
+  \-- NT_cleft (NT already in the synapse) Piu vicino alla Fullness meno release
+- NT_RRP replenishment
+  \-- ATP
+- CaMicro evolution
+  \-- AP
+  \-- ATP
+  \-- various pumps
+- NT_cleft evolution
+  \-- NT release
+  \-- NT EEATS (Astro)
+- 
 
 **Tubs:**
 
@@ -120,4 +133,3 @@ container: BEH-PRE
 
   tub_intricated:   
 ```
-