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@@ -404,12 +404,12 @@ episode: CaTracesAccumulationSlow
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### sec: behaviors PRE
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### sec: behaviors PRE
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#### CheckConditions: Context
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#### CheckConditionsPreSec: Context
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Contestualizziamo in maniera Fixed ogni mezzo secondo?
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Contestualizziamo in maniera Fixed ogni mezzo secondo?
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```Gen
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```Gen
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context: CheckConditions
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context: CheckConditionsPreSec
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contained_by: BEH-PRE
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contained_by: BEH-PRE
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in_context: Fixed
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in_context: Fixed
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@@ -21,7 +21,19 @@ Container: BEH-BD
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## BEH-POST: Container
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## BEH-POST: Container
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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.
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The postsynapse is the receiving terminal of a neuron — a specialised patch of membrane on the surface of a dendrite, sitting directly across the synaptic cleft from the presynapse. Its job is to detect the neurotransmitters (NT) released by the presynapse, convert that chemical signal back into an electrical response, and decide — based on the history and pattern of that activity — whether to strengthen or weaken the connection for the future.
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To do this, the postsynapse maintains two types of receptor on its membrane surface. AMPA receptors are the fast responders: when NT binds them, they immediately open and allow sodium ions to rush in, raising the local membrane potential (V_post). NMDA receptors are the coincidence detectors: they can only open fully when two conditions are simultaneously true — NT must be present in the cleft, and the membrane must already be strongly depolarised. Under resting conditions a magnesium ion physically plugs the NMDA channel from the inside, blocking calcium entry. Only a sufficiently large depolarisation can eject this plug. This dual requirement makes NMDA receptors the central logic gate of the postsynapse.
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The depolarisation that clears the NMDA block can come from two sources acting together. Local AMPA activation raises V_post from incoming NT. A back-propagating action potential (bAP) — an electrical echo of the postsynaptic neuron's own firing that travels backward up the dendrites from the cell body — provides an independent boost. When both arrive simultaneously, V_post reaches its maximum and the NMDA gate opens fully. When only one arrives, or when they arrive at different times, the gate stays partially or fully blocked. This coincidence detection is what gives the postsynapse its ability to distinguish meaningful coordinated activity from random noise.
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When the NMDA gate does open, calcium (Ca²⁺) surges into the postsynaptic spine. The size of this surge is the key signal. A large surge — produced by strong, well-timed coincidence — activates molecular machinery that inserts more AMPA receptors into the membrane, making the synapse more sensitive to future NT release. This is long-term potentiation, or LTP: the postsynapse remembers that this connection was recently successful and strengthens it. A weak or poorly timed surge — produced when the presynapse fired but the postsynaptic neuron was not ready — activates a different pathway that removes AMPA receptors, weakening the connection. This is long-term depression, or LTD. The amplitude of Ca²⁺ in the spine is therefore the plasticity controller: it translates the timing of electrical events into lasting structural change.
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But the postsynapse does not only look forward. If Ca²⁺ in the spine remains elevated for too long — a sign that incoming activity is excessive — the postsynapse synthesises a chemical called an endocannabinoid (eCB) and releases it retrogradely across the cleft. This signal travels backward to the presynapse and suppresses the very channels that are driving the excess activity. This is the postsynapse telling the presynapse to ease off: a retrograde brake, operating on the seconds timescale, that protects the spine from being overwhelmed.
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After every response, ion gradients must be restored. Sodium that entered through AMPA receptors must be pumped back out by Na/K-ATPase. Calcium that entered through NMDA receptors must be pumped out of the spine by dedicated calcium pumps. Both processes consume ATP continuously, and their cost scales directly with how active the synapse has been.
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The ATP supply comes from the same astrocyte that serves the presynapse — a shared glucose budget that both sides draw from simultaneously. Under sustained high-frequency activity, this shared supply can be exhausted. When postsynaptic ATP falls, the calcium pumps slow and Ca²⁺ begins to accumulate in the spine even between genuine coincidence events. This accumulation looks, to the postsynapse, indistinguishable from real overactivity: the eCB threshold is crossed, the retrograde signal fires, and the presynapse is silenced — not because it was genuinely excessive, but because the postsynapse has lost the ability to clear calcium fast enough to distinguish signal from noise. This false trigger is a desperate survival mechanism. By silencing the presynapse, NT input stops, NMDA gates close, the calcium load drops, the pumps have a chance to recover, and the synapse pulls back from the edge of excitotoxic collapse.
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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.
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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.
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@@ -61,11 +73,13 @@ This is the "Hidden Master" that determines if the other two loops are allowed t
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- **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.
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- **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.
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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.
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---
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---
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### The Critical Connection with the presynapse
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### The Critical Connection with the presynapse
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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.
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The system is beautifully asymmetric. While the presynapse is built to **supply** signal, the postsynapse is built to **filter** it.
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```Gen
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```Gen
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container: BEH-POST
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container: BEH-POST
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@@ -89,12 +103,12 @@ container: BEH-POST
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### ms: behaviors POST
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### ms: behaviors POST
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#### CheckConditions:Context
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#### CheckConditionsPostMs:Context
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Contestualizziamo in maniera Fixed ogni mezzo secondo?
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Contestualizziamo in maniera Fixed ogni mezzo secondo?
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```Gen
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```Gen
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context: CheckConditions
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context: CheckConditionsPostMs
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contained_by: BEH-POST
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contained_by: BEH-POST
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in_context: Fixed
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in_context: Fixed
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