commento ASTRO

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2026-03-26 12:56:17 +01:00
parent 5475f8df48
commit 41dac53204
2 changed files with 33 additions and 6 deletions
+6 -5
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@@ -23,8 +23,6 @@ container: BEH-AXO
## BEH-PRE: Container
**High level description**:
The presynapse is the sending terminal of a neuron — a small bulb at the tip of an axon whose job is to release chemical signals, called neurotransmitters (NT), into the synaptic cleft, the narrow gap that separates it from the receiving neuron's postsynapse.
To do this, the presynapse maintains a stockpile of NT packed inside small membrane bubbles called vesicles. These vesicles are organised in two pools: a reserve pool (RP), which is the deep storage, and a readily-releasable pool (RRP), which is the small set of vesicles docked at the membrane and ready to fire immediately. When a spike arrives — an electrical pulse called an action potential — it briefly opens specialised calcium channels (VGCCs) in the membrane. Calcium (Ca²⁺) rushes in, and the sudden local surge of calcium triggers the docked vesicles to fuse with the membrane and pour their NT into the cleft.
@@ -90,9 +88,9 @@ In this first comprehension, we decide to simplify:
The simplification impies that:
- Removing CDI and mGluR means Ca²⁺ concentration and NT_cleft are now the only two variables controlling release rate. This is cleaner and matches your fast/medium/slow framing directly — the release rate table from earlier becomes the core logic of the ms loop.
- Removing CDI and mGluR means Ca²⁺ concentration and NT in the cleft are now the only two conditions controlling release rate.
- Removing ATP removes the metabolic silencing cascade entirely. The mins loop now only does one thing: replenish the NT reserve. If you want the synapse to still be able to fail under sustained firing, the mechanism would have to come from NT depletion alone (RP exhausted, nothing to replenish) rather than from pump failure and Ca²⁺ accumulation.
- Removing ATP removes the metabolic silencing cascade entirely. The mins loop now only does one thing: replenish the NT reserve. If we want the synapse to still be able to fail under sustained firing, the mechanism would have to come from NT depletion alone (RP exhausted, nothing to replenish) rather than from pump failure and Ca²⁺ accumulation.
- "Ca²⁺ cleared slowly" replaces PMCA, NCX, and SERCA with a single exponential decay. This means Ca²⁺ will still accumulate under high firing if the decay is slow relative to the spike rate, which preserves some of the residual-Ca²⁺ dynamic even without the full pump machinery.
@@ -123,8 +121,11 @@ The simplification impies that:
**— mins:**
- Glucose level sets conversion_efficiency
- Glucose level sets base conversion_efficiency
- If astrocyte wave was triggered → conversion_efficiency boosted temporarily
- Glutamine shuttle refills NT reserve from astrocyte store
(faster if wave active, baseline if not)
- Wave boost decays back to baseline over subsequent cycles
**Tubs:**