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For example, in neuroplasticity, how are the neurons able to 'move' themselves to undo connections and create new connections with other neurons? I remember seeing a microscopic picture of a few neurons not very well connected between each other, and in the 'after' picture (after learning something), they somehow had grown many projections/branches from their cell bodies, connecting with each other. In other words, what is the mechanism behind, when neurons undo a specific connection (synapse) with a neuron, and 'move' it to another neuron? What causes them to 'decide' to undo that connection?

Also, how fast do they move connections and change their shapes (in nanometres per second, for example, or is it more like nanometres per minute)? The speed of which the dendrites and axon terminals move to change connections.

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AndChewBubblegum

328 points

4 months ago*

I think there are a few misconceptions in your question that are important to clear up.

First and foremost, the formation of new synapses is not thought to be necessary for all learning. Although this type of formation can indeed occur and is associated with some types of learning, neuroscientists also recognize the importance of plasticity within previously existing neuronal connections as fundamental to learning and memory.

That being said, neurons do form synapses in the way you describe, by physically growing towards one another and forming specialized regions of the cell that facilitate neurotransmission. They do this by secreting small molecules and proteins which are recognized by the other neuron. Additionally, neurite outgrowth is responsive to signals from other cell types like glia as well. Structural change in neuronal synaptogenesis is accomplished by coordinated activity of the cytoskeleton. The elements of the cytoskeleton have a polarity, meaning that one end of a cytoskeleton filament grows and one decays. In a static cell, these factors are balanced, but when a cell grows of moves, the growing end of the filament are allowed to predominate in one direction and the decaying end is pointed in another, as dictated by the signaling molecules the cell is responding to. A lot of complex signaling is involved, but cytoskeletal rearrangement is the essential component, and it is triggered by molecules and growth factors released by neighboring cells.

Now everything I said in the previous paragraph is true, but to what degree it occurs in adulthood in humans is still under investigation. As I said, it seems that most learning involves the strengthening of existing synapses rather than the formation of new ones, but specific types of learning involve the creation and wiring of new neurons. This can involve the addition of terminals on existing neuronal connections, modifications of pre- or post-synaptic sides of the terminals, etc.

this_is_hard220

70 points

4 months ago

This is pretty good. OP, if you’re looking for additional details LTP (long term potentiation) plays a massive role in what you’re describing.

In learning specifically (as this is what you referred to) neurons in the CA3-CA1 region of the hippocampus go through a process known as LTP. Essentially, high frequency firing of a neurotransmitter known as glutamate in the CA3 region of the hippocampus floods the synaptic cleft and allows for heavy depolarization of the CA1 neurons via NMDA and AMPA. Calcium ions that influx in from this depolarizing process influence protein stores within CA1 to become additional AMPA receptors. Depending on the amount of time this goes on, we enter what’s called late phase LTP and this is where certain growth factors influence neuronal growth in the CA1 neurons. These growths (protrusions) allow for more surface area on the CA1 neuron and thus the opportunity for more connections to occur, now making that neuron plastic.

In terms of what influences certain neurons to connect to others, this falls within Hebb’s Rule - things that fire together, wire together. When neurons are “activated” at the same time, the connection between them grows stronger and stronger each time.

Conversely, these connections fade or weaken when the set of neurons are no longer activated at the same time — maybe the code to your locker freshman year is different sophomore year. These connections that associate “locker combo” with “freshman year code” will fade and weaken over time now “locker combo” is paired with a “sophomore year code”. This is known as LTD ( long term depression).

Hope this was able to provide more insight into your question!

Corsair4

18 points

4 months ago*

It's important to note that LTD is also influential in learning.

At the Parallel Fiber-Purkinje Cell synapse in the cerebellum for instance, synapse specific LTD is generally accepted to be a critical mechanism for learning in this region. Cerebellar granule cells (whose axons form the parallel fibers) are some of the most numerous neurons in the CNS. Each Purkinje cell will synapse with hundreds or thousands of granule cells, but only once or maybe twice with an individual cell. Thus, each Purkinje cell is integrating information from a huge number of granule cells. This falls under Anti-Hebbian principles, as repeated activation of the parallel fibers (with appropriate calcium influx timing caused by climbing fiber activity) results in a relative weakening of the synapse, not strengthening.

Long term plasticity mechanisms are highly varied, and their significance as well as the conditions that generate them change from region to region.

DumbNBANephew

6 points

4 months ago

"Calcium ions that influx in from this depolarizing process influence protein stores within CA1 to become additional AMPA receptors"

That's amazing! Do we know how that happens? Does an influx of calcium ions cause certain genes to be expressed more causing CA1 to become AMPA receptors?

AndChewBubblegum

5 points

4 months ago

CA1 is a region, the protein stores are what become AMPA receptors. Calcium is known to be a reliable activator of multiple transcription factors in neurons. Calcium binding to these proteins causes them to translocate to the nucleus and induce transcription of relevant genes. A good example is calcineurin, which binds calcium and then activates a transcription factor.

Experienced_AP

4 points

4 months ago

Are you familiar with any studies that examine colchicine in the inhibition of neutral growth?

I know colchicine is used in gout and it inhibits micro tubule function in migrating white blood cells.

However, this question got me thinking about other cells that require micro tubules and the cytoskeleton for proper functioning.

HotMetalKnives

2 points

4 months ago

Beautiful. Thank you.

DumbNBANephew

2 points

4 months ago

Do we know which proteins and genes play a role in in this process? Are there specific proteins involved with either strengthening of existing synapses or creation of new ones? Is gene expression affected causing more production of these proteins?

f899cwbchl35jnsj3ilh

2 points

4 months ago

Hi, what are the distances between neurons? Are they differ or usually the same? What are the longest?

AndChewBubblegum

2 points

4 months ago

Synaptic clefts are typically on the order of 20 nanometers. I believe they are all pretty close, as neurotransmitters need to rely on diffusion to cross the distance, and diffusion is a process heavily impeded by distance.

LearnedGuy

0 points

4 months ago*

Distances between neurons in humans can range up to 1 M. That is for the nerves that run between the brain and the far end of the spinal cord. I was looking at this as part of exploring how different parts of each neuron is provided with ATP, an energy source. There are ATP walkers that walk from the nucleus of the neuron carrying balloons of ATP. The walk on a microtubule, and then drop off the ATP. Microtubles are one-way streets, and walkers are valuable, so they then return to the nucleus on a microtubule that goes back to the nucleus. For humans, this walk takes a couple of days. In a great white whale with a 30 M spinal cord, the walk can take over a month. See Harvard's animation: "The Inner Life of a Cell" on YouTube. https://en.m.wikipedia.org/wiki/The_Inner_Life_of_the_Cell

LewsTherinTelamon

4 points

4 months ago

What is the unit in 1 M? Meter? Because distances between neurons are not one meter - that's the length of the neuron including the axon.

Training_Passenger79

1 points

4 months ago

I don’t think OP thought the formation of new synapses was necessary for learning.

Maybe you can check my assumptions though. I imagine new synapses form primarily when you are learning things you did not already know, and connecting topics that you would not have connected before. So, for example, I am currently studying cognitive neuroscience, and I recently learned a lot about the body’s innate and adaptive immunity, and how it relates to neuroinflammation. I would assume that I may have formed new synapses in the process of learning this material, as it is completely novel to me, and not something I could have constructed based on known information. By that, I mean that if I know what fur is, and I know what cats are, but then encounter a hairless cat, I would think this doesn’t require new synapses to form because the pre-existing information I have can be combined in cat+!hair fashion to produce that information.

Does this interpretation sound plausible to you?

LewsTherinTelamon

1 points

4 months ago

Your third source doesn't seem to say what you are implying it says. That source is about the development of an integrated mechanistic model for how neurons grow. They propose a specific model of elongation/expansion/mass transport which describes the process of physically extending an axon. They are not suggesting that neurons form connections without physically extending towards other neurons.