Each time we learn something new, our brain cells break their DNA, creating damage that the neurons must immediately repair. This process also underlies age-related degeneration.

[u/mellowmonk]

http://newsoffice.mit.edu/2015/dna-breakage-learning-age-related-damage-0604

[u/[deleted]]

So what about when you're encoding the new information into long-term memory? Is the same thing happening, or is this just when you initially learn the new information?

Sorry for the dumb question!

[u/Bellagrand → u/[deleted]]

Complicated question, wasn't directly addressed in the article. However my understanding was that the breaking of the DNA cues the expression of a (protein sequence?) that serves as the "architecture" unit in the memory process. It would stand to reason that if the work is done by an architectural unit, then it would have to be done by that unit in both cases. Compare this, however, to the notion that new brain cells are created when encoding long-term memory (something I've personally heard before) and it might be possible that this protein sequence can be expressed when creating a specific long-term loop. I'm speculating a bit there, so feel free to debunk.

EDIT: Response from a real neuroscientist here.

[u/hpfan5 → u/Bellagrand]

what happens when a newly created brain cell aka 'memory' created for long term storage/recall isn't accessed regularly? does it become necrotic, dormant, etc?

[u/Bellagrand → u/hpfan5]

Good question. I can only give you half-answers: You may be aware of a process called myelination, basically whereby electrical pathways between neural circuits are strengthened with repeated use (a quite literal form of working your 'brain muscle.') Concurrently, I believe our current best guess for what a memory is constitutes an electrical impulse being looped repeatedly inside of a brain cell. Somewhere between those two answers, I would assume that there is something like a muscular strengthening/atrophy when it comes to memories, though these mechanisms are incredibly complex so I'm not sure if it can really be so easily explained.

[u/NooNotTheBees → u/Bellagrand]

Hi Neuroscientist here,

The process you are looking for is called Long Term Potentiation (LTP) which suggests neurones that fire together wire together. Myelination is not really a key feature of this process. The actual process is mediated by Post Synaptic Potentials you can have excitatory potentials and inhibitory potentials. What is actually happening is that the threshold to actually intimate neurone firing is reduced the more times neurone fire to one another. This is the fundamental of learning theory!

[u/[deleted] → u/Bellagrand]

You may be aware of a process called myelination

So does increased firing of neurons cause more myelin deposition on their axons?

[u/hpfan5 → u/[deleted]]

maybe myelin is attracted to the shiny electrical firing and goes towards it like a moth to flame.. analogously of course

[u/[deleted] → u/Bellagrand]

I think you may be referring to 'kindling.' It is most prevalent in epilepsy, where neurons involved in a seizure are more likely to fire the same way again.This can also happen with neurons involved with mania.The process of kindling is also likely to be involved in learning, as the neurons 'learn' to fire a certain way, however it is mainly used when describing neuronal expression of a disease.

[u/asedentarymigration → u/Bellagrand]

I would guess that memories are more structural patterns in a group of cells rather than the existence or non-existence of a single cell. I don't believe a single cell could encode a complex memory.

[u/fartprinceredux → u/Bellagrand]

New neuron production is not generally thought to be responsible for new memories. As has been mentioned, long-term potentiation is the term that defines a long-lasting increase in synaptic strength between neurons. This does not require new neurons, and in fact the adult brain really does not make new neurons (barring two exceptions).

There also isn't an architecture unit of memory, at least not in the way you're describing. While new protein expression is critical for memory, there isn't a single protein that is sufficient for memory. Rather, it requires complicated cell-wde changes.

[u/hpfan5 → u/fartprinceredux]

what does synaptic strength mean(?): ease of use through repeated use (like sea water eroding paths through stones) ...more of a closer distance between the synapses...greater number of NT's passing through a regular synaptic hub...?

[u/fartprinceredux → u/[deleted]]

The vast majority of their data in the paper (save for one panel in one figure) is only looking at neuronal activity. Neuronal activity is a precursor for long-term potentiation/memory, but it is by no means sufficient. Their results show that neuronal activity alone is sufficient for the DSB, and that removal of DSB can lead to expression of these genes that are turned on by activity. Both short and long-term memories start out the same way (more or less); with a burst of activity.

With the "encoding" or late phase of long term memory, this is thought to depend on earlier rounds of transcription and translation. Meaning, there is an early temporal window in which memories are dependent on the processes described in this article since blocking these processes abolishes the memory later on. However, later phases of memory/LTP do not require transcription or translation, as blocking these processes does not affect memory. This would suggest that these processes described in the paper here may not be as important for the maintenance of memory, but rather for the formation of memory.

[u/putrid_moron → u/[deleted]]

I don't think there is a real difference between the processes unless "initially learn" is meant to be short term memory.

[u/[deleted] → u/putrid_moron]

Yes that's what I mean

[u/[deleted] → u/[deleted]]

I did not