# Synaptic Permanence

**URL:** <https://discourse.numenta.org/t/synaptic-permanence/1848>\
**Category:** General Neuroscience\
**Tags:** permanence, synapses\
**Created:** [January 28, 2017, 9:54pm UTC](https://discourse.numenta.org/t/synaptic-permanence/1848 "2017-01-28T21:54:48Z")\
**Posts on this page:** 4\
**Page:** 2

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**Author:** ![subutai](https://yyz2.discourse-cdn.com/flex030/user_avatar/discourse.numenta.org/subutai/32/106_2.png) [@subutai](https://discourse.numenta.org/u/subutai)\
**Post date:** [January 31, 2017, 9:59pm UTC](https://discourse.numenta.org/t/synaptic-permanence/1848/21 "2017-01-31T21:59:29Z")

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> [@vpuente](#):
>
> I have a related “conceptual” problem: It is biologically plausible the current forgetting model in CLA?
> 
> The problem I have, is how punishment in the current CLA model relates the biology. According this code a predicted but not active cell will imply a punishment to the “optimistic” active synapses.
> 
> I couldn’t find any bio reference for that.

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).

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**Author:** ![vpuente](https://yyz2.discourse-cdn.com/flex030/user_avatar/discourse.numenta.org/vpuente/32/4115_2.png) [@vpuente](https://discourse.numenta.org/u/vpuente)\
**Post date:** [February 1, 2017, 9:37am UTC](https://discourse.numenta.org/t/synaptic-permanence/1848/22 "2017-02-01T09:37:08Z")

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

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**Author:** ![sebjwallace](https://yyz2.discourse-cdn.com/flex030/user_avatar/discourse.numenta.org/sebjwallace/32/6411_2.png) [@sebjwallace](https://discourse.numenta.org/u/sebjwallace)\
**Post date:** [February 1, 2017, 8:23pm UTC](https://discourse.numenta.org/t/synaptic-permanence/1848/23 "2017-02-01T20:23:13Z")

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> [@jhawkins](#):
>
> Spines vary in thickness. Some people had suggested that thick-spined synapses release more transmitter. But I once read a paper that argued that this wasn’t really the case. That paper, which I haven’t been able to find again, suggested that thick spines were more indicative of how “permanent” the synapse was.

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.

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**Author:** ![ollivier26](https://yyz2.discourse-cdn.com/flex030/user_avatar/discourse.numenta.org/ollivier26/32/1088_2.png) [@ollivier26](https://discourse.numenta.org/u/ollivier26)\
**Post date:** [February 3, 2017, 6:06pm UTC](https://discourse.numenta.org/t/synaptic-permanence/1848/24 "2017-02-03T18:06:34Z")

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Hi,  
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](http://neurosciencenews.com/sleep-brain-reset-6047/), 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.

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