ocrampal/organism
1
0
Fork 0
Code Issues Pull Requests Actions Packages Projects Releases Wiki Activity

Update 2026-06-04-modulation-of-future-behavior.md

Browse Source
This commit is contained in:
ocrampal
2026-06-05 16:29:52 +02:00
parent c875fd975e
commit 48979a3d31
1 changed files with 3 additions and 1 deletions
Download Patch File Download Diff File Expand all files Collapse all files
elements/astrocyte/appunti/2026-06-04-modulation-of-future-behavior.md
+3 -1
View File
@@ -24,7 +24,9 @@ At the slow scale, all three compartments track their own physical architecture:
## Fast scale: what happens spike by spike ## Fast scale: what happens spike by spike
Every action potential sets off a precise sequence across all three compartments simultaneously. The presynapse converts the electrical event into a chemical wavefront: calcium floods in, drives probabilistic vesicle release from the readily-releasable pool, and leaves a residual trace that biases the next release upward if spikes keep arriving and downward if they stop. The amount of glutamate released fills the cleft and begins diffusing outward. Every action potential sets off a precise sequence across all three compartments simultaneously.
The presynapse converts the electrical event into a chemical wavefront: calcium floods in, drives probabilistic vesicle release from the readily-releasable pool, and leaves a residual trace that biases the next release upward if spikes keep arriving and downward if they stop. The amount of glutamate released fills the cleft and begins diffusing outward.
The astrocyte responds in two parallel arms the moment glutamate spills beyond the cleft boundary. The first arm activates astrocytic mGluR5 receptors via a Gq cascade, triggering an internal calcium rise that is directly proportional to how much glutamate has escaped — this calcium rise drives D-serine release, widening the postsynaptic NMDA detection window. The second arm simultaneously activates presynaptic mGluR2/3 receptors via Gi, suppressing adenylyl cyclase and reducing vesicle release probability — a direct autoinhibitory brake on the very source of the overflow. These two arms run in opposite directions from the same trigger: the astrocyte brakes the presynapse while amplifying the postsynaptic learning window at the same time. The astrocyte responds in two parallel arms the moment glutamate spills beyond the cleft boundary. The first arm activates astrocytic mGluR5 receptors via a Gq cascade, triggering an internal calcium rise that is directly proportional to how much glutamate has escaped — this calcium rise drives D-serine release, widening the postsynaptic NMDA detection window. The second arm simultaneously activates presynaptic mGluR2/3 receptors via Gi, suppressing adenylyl cyclase and reducing vesicle release probability — a direct autoinhibitory brake on the very source of the overflow. These two arms run in opposite directions from the same trigger: the astrocyte brakes the presynapse while amplifying the postsynaptic learning window at the same time.