`Voltage-Context` is labelled as an Episode but contains sub-episodes — it should be a Context. Same for `NMDA-Coincidence` and `Ca-Dynamics & ATP-Drain`. You have used Episode and Context interchangeably in a few places; the distinction matters for the specification: a Context sets the conditions, an Episode is a named outcome within those conditions.
`Vpost_Maximum` lists `V_bAP full OR (g_AMPA full AND V_bAP medium)` — this is correct Boolean logic and should be kept exactly as written. It captures the two ways the postsynapse can reach maximum depolarisation: the bAP alone if it is strong enough, or AMPA plus a partial bAP together.
`AMPA_Population_Increase` correctly gates on `ATP_level_post NOT empty` — LTP requires ATP for CaMKII phosphorylation and receptor trafficking. LTD does not have the same gate in your spec. This is slightly asymmetric — LTD (receptor internalisation via endocytosis) is also ATP-dependent, though less so than LTP. Worth noting.
`Plasticity_LTD` covers `Ca_post_history medium` but does not cover the case where `Ca_post_history` is empty — a completely silent synapse also weakens over time (homeostatic depression). This can be left as a gap or named explicitly.
The bAP needs new parameters and state variables in the model before it can be expressed as a fully implemented behavior. I will add those inline as `[GAP — to implement]` markers so the spec is complete even where the code is not yet written.
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:
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
