added stp/stD observed behaviors

neuron/BEH-AXO.md

@@ -91,6 +91,9 @@ The presynapse does not release blindly. Its behaviour is governed by three inte
 - NT added to cleft
 - NT_released_this_window accumulates (feeds mGluR and IP3 in seconds loop)
 - NT passively diffuses out of cleft (physical, not astrocyte)
+- Observed behaviors:
+-- STD: exhaustion of NT momentarly stops presynapse from releasing NT
+-- STP: Ca2+ left in the presynapse beteween spikes primes next NT release.
 
 — seconds:
 
@@ -140,6 +143,9 @@ The simplification impies that:
 - NT released into cleft — rate determined by Ca²⁺ level and NT already in cleft
 - NT released accumulates (feeds sec behavior)
 - NT passively diffuses out of cleft
+- Observed behaviors:
+-- STD: exhaustion of NT momentarly stops presynapse from releasing NT
+-- STP: Ca2+ left in the presynapse beteween spikes primes next NT release.
 
 **— seconds:**
 

neuron/appunti/2026-03-30-behavior-POST.md

@@ -301,3 +301,103 @@ Structural-Update: Context
 ---
 
 ---
+
+## short term
+
+Short-term potentiation (STP) and short-term depression (STD) are distinct from LTP/LTD in a fundamental way: they are **temporary** changes that last seconds to minutes and leave no lasting structural trace. They do not require the postsynapse at all — they are entirely presynaptic phenomena in most cases, and they operate on a completely different mechanism.
+
+---
+
+**What they are and where they live**
+
+Short-term plasticity is driven by the **history of presynaptic Ca²⁺** and **vesicle pool state**, not by postsynaptic coincidence detection. The table we just built describes long-term plasticity — structural changes to AMPA density driven by Ca_post. Short-term plasticity describes transient changes to **how much NT the presynapse releases** on the next spike, driven by what happened on the last few spikes.
+
+There are two opposing forms:
+
+**Short-term potentiation / facilitation** — if a spike arrives shortly after the previous one, residual Ca²⁺ from the first spike has not fully cleared. The next spike adds to this residual, producing a larger Ca_post microdomain and therefore a higher release probability. The synapse releases more NT on the second spike than the first. This is already partially captured in the presynaptic model through `Tr_Ca` — elevated calcium trace from recent activity speeds up RRP recruitment and effectively increases release efficiency.
+
+**Short-term depression** — if spikes arrive rapidly, the RRP depletes faster than it can be refilled. Each successive spike releases fewer vesicles because there are fewer available. NT release drops with each spike in a burst. This is already the core of CASCADE 1 in the presynaptic model — RRP depletion under high firing rate.
+
+---
+
+**Where they fit in the model**
+
+Both are already implicitly present in the presynaptic ms and seconds loops:
+
+```
+Short-term facilitation:
+  Residual Ca_micro from spike N
+  → elevated Ca_micro at spike N+1
+  → higher release fraction in deterministic_release (Hill curve)
+  → more NT per spike
+  → decays as Ca_micro clears between spikes (tau ~100-200 ms)
+
+Short-term depression:
+  Rapid firing depletes N_RRP
+  → fewer vesicles available per spike
+  → released_NT falls
+  → recovers as RP→RRP recruitment refills (seconds timescale)
+```
+
+The timescale of each depends on parameters already in the model:
+
+| Form         | Timescale  | Driven by         | Recovery                |
+|--------------|------------|-------------------|-------------------------|
+| Facilitation | 100-500 ms | residual Ca_micro | Ca²⁺ clearance rate     |
+| Depression   | seconds    | RRP depletion     | RP→RRP recruitment rate |
+
+---
+
+**What is missing from the current model**
+
+The model captures both implicitly but does not name them as behaviours. Two things are genuinely absent:
+
+**Augmentation** — a slower form of facilitation lasting 5-10 seconds, driven by residual Ca²⁺ accumulating in the presynaptic terminal across many spikes. It is distinct from spike-by-spike facilitation and would require a second, slower Ca²⁺ trace with `tau ~5000 ms`. The current `Tr_Ca` with `tau = 1000 ms` is between the two — it captures some augmentation but not cleanly.
+
+**Post-tetanic potentiation (PTP)** — an even slower presynaptic enhancement lasting minutes after a high-frequency burst, driven by protein kinase C activation from sustained Ca²⁺ elevation. This is a presynaptic phenomenon that looks like LTP from the outside but has no postsynaptic component and no structural change. It would require a third, very slow trace variable.
+
+---
+
+**How they interact with the LTP/LTD table**
+
+Short-term and long-term plasticity operate on the same synapse simultaneously but independently:
+
+```
+Spike arrives
+  → short-term: how much NT releases THIS spike  (presynaptic, ms-seconds)
+  → long-term:  does the synapse get stronger or weaker PERMANENTLY  (postsynaptic, mins-hours)
+```
+
+A synapse can be undergoing LTD (slowly losing AMPA receptors over minutes) at the same time as it is showing short-term facilitation (releasing more NT per spike due to residual Ca²⁺). The two processes do not interfere — they act on different variables through different mechanisms.
+
+The important implication for your model is that **the LTP/LTD table we built describes what happens to** `g_AMPA_baseline` **over minutes**. Short-term potentiation/depression describes what happens to `released_NT` over milliseconds to seconds. They are different outputs of the same synapse, running in parallel.
+
+If you want to add short-term plasticity explicitly to the behaviour specification it would live entirely in the presynaptic ms and seconds loops as named episodes of existing variables:
+
+```
+— ms (presynapse, short-term plasticity):
+
+ShortTermFacilitation: Episode
+  — residual Ca_micro > 0 at next spike arrival
+  — release_frac in deterministic_release elevated above baseline
+  — decays as Ca_micro clears (tau ~100-500 ms)
+  — more NT per spike than at rest
+
+ShortTermDepression: Episode
+  — N_RRP depleted by rapid successive spikes
+  — release_frac unchanged but N_RRP reduced
+  — fewer absolute vesicles released per spike
+  — recovers via RP→RRP recruitment (seconds)
+
+— seconds (presynapse, short-term plasticity):
+
+Augmentation: Episode  [GAP — not yet modelled]
+  — requires second slow Ca2+ trace (tau ~5000 ms)
+  — elevated release probability for 5-10 s after burst
+  — distinct from spike-by-spike facilitation
+
+PostTetanicPotentiation: Episode  [GAP — not yet modelled]
+  — requires very slow trace (tau ~minutes)
+  — elevated release probability for minutes after tetanus
+  — presynaptic only, no postsynaptic component
+```