varie

elements/neuron/README.md

@@ -329,6 +329,55 @@ In this model we decide to simplify:
 - We do not model subthreshold oscillations — VSOMA is a simple leaky integrator
 - We do not model somatic ATP
 
+**Simplified verifiable behaviors**:
+
+— ms:
+
+- Resting at -70 mV: Leak channels + pumps (keep at resting)
+- VDB Depolarization : ~1-2 ms: Na⁺ enters (some VGSCs open)
+- Opened VGSC and then remain closed for a refractory period
+- Spike if depolarized above threshold: to -50 mV
+- Ca2+ enter
+- Repolarization to -70 mV:  ~1-2 ms: K⁺ exits (VG K⁺ channels open) ← NOT pumps!
+- After-hyperpolarization: ~5-20 ms: K⁺ channels still open
+
+— secs:
+
+- Return to exact -70 mV: ~100-1000 ms: Na⁺/K⁺ pumps restore gradients
+- Ca2+ accumulation
+
+— mins:
+
+- VGSC modulation
+
+---
+
+**G expression**:
+
+— ms:
+
+- based on VDB, VGSC open and let Na+ in. VGSG then go into refractory
+- if Na fullness then ApCtx. Here the threshold is based only on the integration of Na+
+- increase SpikeTrainTraces (fast at spike)
+- increase Ca2+ traces
+- decrease Na: fast pump which decreases Na+, we do not model K+
+-- there is a tug of war between Na entering and exiting. Na can reach fullness only if VDB increases fast (derivative)
+- there are 2 context: ApCtx and SomaRefractory imlemented with timers and tunable
+- decrease SpikeTraintraces slow, only if away from spiketrain this is empty
+
+- Tune:
+-- The threshold is tuned during the spiketrain. Low threshold at rest, to increase sensitivity, threshold increase during spike to increase discrimination
+
+— secs:
+
+- SpikeTrainTraces
+
+— mins:
+
+- Tune:
+-- refractory lenght
+
+
 The simplifications imply that:
 
 Removing the axon hillock as a separate compartment means the threshold comparison is applied directly to VSOMA rather than to a spatially distinct zone with its own channel density. In biology the hillock has a lower threshold than the soma body because of its higher Na⁺ channel density — this gradient is absent here. A single fixed threshold applied to VSOMA is a reasonable approximation for a single-compartment model, but it means the model cannot capture phenomena that depend on the hillock's spatial separation from the dendritic integration zone, such as the ability of strong distal dendritic inputs to bypass somatic inhibition.
@@ -371,6 +420,20 @@ In this model we decide to simplify:
 - We do not model bAP distance attenuation — all spines receive the bAP at full amplitude regardless of their position
 - We do not model structural plasticity — spine neck widening and retraction are not implemented
 
+— ms:
+
+- Each active spine contributes VPost (EPSP) to VDB
+- VDB decays passively each ms
+  
+— secs:
+
+- nothing in the simplified model
+
+— mins:
+
+- nothing in the simplified model  
+  (structural remodelling of spine neck geometry under LTP/LTD would live here if added later)
+
 The simplifications imply that:
 
 - Removing spine neck resistance means all spines contribute equally to V_dend regardless of their geometry or location. The physical basis of synaptic weighting by dendritic position is lost. All EPSPs are treated as equivalent inputs to the shared pool.