From d8281e9b76c4a5a9eefc04bebecbc4fb84ea19d9 Mon Sep 17 00:00:00 2001 From: ocrampal Date: Fri, 3 Apr 2026 14:35:32 +0200 Subject: [PATCH] added stp/stD observed behaviors --- neuron/BEH-AXO.md | 6 ++ neuron/appunti/2026-03-30-behavior-POST.md | 102 ++++++++++++++++++++- 2 files changed, 107 insertions(+), 1 deletion(-) diff --git a/neuron/BEH-AXO.md b/neuron/BEH-AXO.md index 50bb4f5..2d0397d 100644 --- a/neuron/BEH-AXO.md +++ b/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:** diff --git a/neuron/appunti/2026-03-30-behavior-POST.md b/neuron/appunti/2026-03-30-behavior-POST.md index 0a806aa..6d04a85 100644 --- a/neuron/appunti/2026-03-30-behavior-POST.md +++ b/neuron/appunti/2026-03-30-behavior-POST.md @@ -300,4 +300,104 @@ Structural-Update: Context --- ---- \ No newline at end of file +--- + +## 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 +``` \ No newline at end of file