Synaptic Permanence



My current favorite theory for that particular effect is that whenever there is an NMDA spike, all the synapses in that segment always undergo a very small decay. Then, if the cell actually initiates an action potential, the synapses get reinforced (potentiated, via the back action potential). This turns out to have the identical net effect as that piece of code.

I don’t know of direct biological evidence for the first part (the decay) but some neuroscientists I have spoken to say it is quite plausible. There is already evidence for the second part in this paper:

[1] 1. A. Losonczy, J. K. Makara, J. C. Magee, Compartmentalized dendritic plasticity and input feature storage in neurons. Nature. 452, 436–41 (2008).


Thanks Subutai. Ouch… I missed that this paper was in the Mendeley group :frowning: )


It is interesting - I’ve just been reading about dendritic spines and it seems there is a good number of resources that support the idea of permanence, however they tend to use the word ‘stability’ as they go through the morphological phases of filopodia, thin, stubby, then mushroom (being the most stable). Then reversing in LTD.


I remember a paper talk about : Bigger Spines let pass more neurotransmitter receptors.

So bigger spine = synapse with more receptors

And according to this paper, synapse not permanent shrink by nearly 20 percent each night (so 20 percent less receptors).

So, synapse with more receptors last longer before reach a threshold and be pruned.

So, thick-spined synapses release more transmitter and last longer.