varie

elements/neuron/README.md

@@ -447,6 +447,32 @@ In this comprehension we decide to simplify:
 - We do not model Desensitization_level — receptor availability is assumed constant
 - We do not model Ca²⁺ clearance detail — Ca_post decays with a single slow term
 
+— ms:
+
+- NT arrives in cleft → AMPA receptors bind NT (receptor availability constant, no desensitization)
+- V_post rises with AMPA conductance, decays passively each ms
+- bAP arrives → V_post receives additional depolarisation boost
+- NMDA gate checks coincidence: NT_cleft AND V_post both non-zero
+- Mg_block_removal = V_post / (V_post + V_NMDA_half) — sigmoid of V_post
+- _Ca2 enters spine via NMDA: Ca_post += k_NMDA × NT_cleft × Mg_block_removal
+- Ca_post decays slowly each ms (single exponential, no pump detail)
+- Ca_post_history updated every ms (feeds seconds loop)
+- V_post_history updated every ms (retained for reference)
+
+— seconds:
+
+- Ca_post_history mean computed over past 2 s
+- eCB synthesised when Ca_post_history mean exceeds eCB threshold
+- eCB_level decays when Ca_post_history mean falls below threshold
+- eCB_level written → read by presynapse as retrograde brake on VGCCs
+- Ca_post_history compared to LTP/LTD thresholds → plasticity tag set
+
+— mins:
+
+- If Plasticity_LTP tagged → AMPA density increases
+- If Plasticity_LTD tagged → AMPA density decreases
+- AMPA density feeds back into receptor_conductance ceiling for next cycle
+
 The simplification implies that:
 
 - Removing ATP removes the false eCB trigger mechanism entirely. The retrograde signal remains but it is always genuine — driven by real Ca_post elevation from NMDA coincidence, not pump failure. The synapse cannot enter the excitotoxic protection cascade.