organism/neuron/BEH-BD.md

# BEH-BD.md

Qui comprendiamo:

- BEH-BD: Dendritic Branch
- BEH-POST: Postsynapsis
- BEH-POST-AMPA: AMPA receptors (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors)

## BEH-BD: Container

**Dendritic Branch**: In questa prima fase, non consideriamo lo spike dendritico come comportamento. Questo limita molto il modello, perche' equipara tutte le Postsinapsi sui tre branch dendritici e non permette di fare in maniera che ad esempio due branch contestualizzino (base activity) e uno faccia scattare il threshold per lo spike somatico.
Qui BEH-DB espande solo i BEH-POST, e' un cavo di collegamento come l'assone

```Gen
Container: BEH-BD
 
 expansion:
  - BEH-POST ( full: 50x, active: 20x, empty: 10x ) 
    modulated_by: DEV-BD-BEH-POST-TUB from DEV-N.md
```

## BEH-POST: Container

The postsynapse is the receiving terminal of the neuron—typically a tiny protrusion called a **dendritic spine**. While the presynapse is a "sending" machine, the postsynapse is a "comparing" machine. Its primary job is to decide if the incoming neurotransmitter (NT) signal is significant enough to warrant a change in synaptic strength, a process it performs by intersecting local chemical signals with global electrical feedback from the cell body.

Like its presynaptic partner, the postsynapse is governed by three interlocking loops—**the $V_{post}$ loop, the $Ca^{2+}$ loop, and the ATP loop**—operating across three distinct timescales.

---

1.The $V_{post}$ Loop: The Fast Gatekeeper (Milliseconds)

This is the primary electrophysiological response, where chemical signals are converted back into electricity.

- **Activation:** When NT arrives in the cleft, it binds to **AMPA receptors**. These act as the primary current drivers. If `NT_cleft` is **Full** and receptors are not in a **Desensitization** state, the $Na^{+}$ influx causes the local membrane potential ($V_{post}$) to rise steeply.

- **The bAP Feedback:** The postsynapse does not work in isolation. It receives a **back-propagating Action Potential (bAP)**—an electrical "echo" sent from the cell body whenever the neuron fires.

- **Coincidence Logic:** On this millisecond scale, the loop computes a logical **AND** operation. If local AMPA-driven depolarization coincides with a somatic bAP, the total $V_{post}$ becomes **Full**. This massive depolarization is the only thing strong enough to kick the magnesium "plug" out of the **NMDA receptors**, allowing the next loop to begin.

---

2.The $Ca^{2+}$ Loop: The Plasticity Controller (Seconds)

This loop translates electrical timing into biological "memory."

- **The NMDA Gate:** $Ca^{2+}$ entry is strictly gated by the NMDA receptor. Unlike the presynaptic VGCCs (which open with any spike), the NMDA channel only opens if it senses both NT (from the presynapse) and high $V_{post}$ (from the bAP).

- **Signaling Fate (LTP/LTD):** The amplitude of the $Ca^{2+}$ surge determines the synapse’s fate. A **Full** surge (perfect coincidence) triggers **LTP**, signaling the astrocyte to help strengthen the synapse. A **Medium** or poorly timed surge triggers **LTD**, weakening the connection.

- **Retrograde Signaling (eCB):** If $Ca^{2+}$ levels remain high for too long, the postsynapse synthesizes **endocannabinoids (eCB)**. This signal travels backward across the cleft to tell the presynapse to stop sending NT. This is the primary safety valve that prevents the postsynapse from being overwhelmed.

---

3.The ATP Loop: The Metabolic Backbone (Minutes)

This is the "Hidden Master" that determines if the other two loops are allowed to function.

- **The Cost of Logic:** The postsynapse is metabolically expensive. The $Na/K$ pumps must work constantly to reset the $V_{post}$ gradient, and the **PMCA pumps** must use ATP to flush out the $Ca^{2+}$ that entered through NMDA channels.

- **The Astrocyte Bridge:** The astrocyte provides the glucose required to replenish ATP. It also performs a "janitorial" service: it clears excess Potassium ($K^{+}$) and Glutamate from the cleft. If the astrocyte is starved of glucose, the **ATP_level_post** drops to **Empty**.

- **The False Trigger (Excitotoxic Protection):** When ATP fails, the $Ca^{2+}$ pumps stop. Even without an NMDA surge, $Ca^{2+}$ begins to "leak" and accumulate in the spine. This creates a **False Trigger**: the high $Ca^{2+}$ level initiates eCB synthesis, silencing the presynapse even though there was no "real" signal. This is a desperate survival mechanism; by tricking the presynapse into silence, the postsynapse stops the influx of ions and buys time for its ATP levels to recover.

---

### The Critical Connection with the presynapse

The system is beautifully asymmetric. While the presynapse is built to **supply** signal, the postsynapse is built to **filter** it. The failure of the ATP loop in the postsynapse is arguably more dangerous; if the postsynaptic pumps fail and the eCB "False Trigger" doesn't fire, the spine will literally digest itself from $Ca^{2+}$ overload.

```Gen
container: BEH-POST

 expansion: 
  - BEH-POST-AMPA ( full: 10x, active: 5x, empty: 2x )
   # modulated_by: TUN-POST-IC # possible/actual

 tub_local:
  - Ca2+ ( full: 60x, active: 30x, empty: 0x )
   # modulated_by: DEV-POST-???-FULL # Full 

  - Nox ( full: 100x, active: 20x, empty: 0x ) # Nitric Oxide (NO):  A gas that diffuses freely.

  - Ecb ( full: 100x, active: 20x, empty: 0x ) # Endocannabinoids (e.g., 2-AG)

 tub_intricated:
  - Nt ( contained_by: BEH-SYN )
  - bAp ( contained_by: BEH-SOMA )
```

### ms: behaviors POST

#### CheckConditions:Context

Contestualizziamo in maniera Fixed ogni mezzo secondo?

```Gen
context: CheckConditions
  contained_by: BEH-POST

  in_context: Fixed
  rf: ( active: 600x )

  condition: NOT (RP empty) AND NOT (RRP full)
    out_context: RPShuttle

  condition: NOT (CaTrace empty) 
    out_context: CaTracesNotEmpty

  condition: NOT (eCB empy) 
    out_context: eCBNotEmpty
```

#### :Episode

## BEH-POST-AMPA: Container

```Gen
container: BEH-POST-AMPA

 tub_intricated:
  - Nt ( contained_by: BEH-SYN )

 context_intricated:
  - bAp ( contained_by: BEH-SOMA )
```

### sec: behaviors POST

### min: behaviors POST

### ms: behaviors AMPA

#### AmpaOpen: Episode

- Timing: < 1 ms
- InContext: Glutamate > FULLNESS
- OutContext: AMPA receptor opening
- Consequence: Na⁺ influx
- Consequence: addition to local depolarization (EPSP) from AMPA activation

```Gen
episode: AmpaOpen
  contained_by: BEH-POST-AMPA

  in_context: NtCapured
  rf: ( active: 1x )

 hypothesis: NOT (Ca2+ full)
  action: [Ca2+ increase]
  trace: None # Se Ca+FULLNESS, lascio tracce di overflow per modulazione DOWN, da capire UP
```

#### Depolarization by bAP

Da ricordare i Dendritic VCGG che si aprono facendo entrare Ca2+ all'arrivo di bAP. In teoria abbiamo 3 Ion Channel.

- Timing: > 1 ms
- InContext: bAP backpropagating action potential
- Consequence: addition to local depolarization (EPSP) from bAP

#### Mg²⁺ NMDA unblock

- Timing: > 1 ms
- InContext: local depolarization (EPSP) > FULLNESS (requires depolarization > -40mV)
- OutContext: NMDA Mg²⁺ unblock

#### Full Ca+ influx by NDMA

- Timing: < 1 ms
- InContext: NMDA Mg²⁺ unblock
- Consequence: Na⁺ influx
- Consequence: addition to local depolarization (EPSP) from Full NMDA activation

#### Upregulation: Observable

- Upregulation: Depolarization relieves NMDA Mg²⁺ block → Ca²⁺ influx amplification

#### Downregulation: Observable

- Downregulation: AMPA desensitization acts as low-pass filter