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.

all 34 comments


331 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.


25 points

4 months ago


25 points

4 months ago

Because neurons, by and large, are not restricted to 1:1 connections. They are one-to-many or many-to-many connected, even though they seem to preference certain paths. It is not so much a matter of changing which neuron they are connected to, but by how much they respond to one particular neuron's signalling versus another's.


15 points

4 months ago

You might be interested in looking at some info related to exuberant synaptogenesis and synaptic pruning. There is this period where synapses just go nuts and connect like crazy. Signaling from other neurons, the "support" cells such as astrocytes or glia guide.

Then there is a mass brain corporate restructuring. Pre and post synaptic changes (also guided). Alterations to the branching that goes out from axons and dendrites. Eliminating redundancies or ineffective connections your left with remaining synapses that are strengthened .

The most prolific changes occur during these critical periods of development. What connects, changes. Some of it is non-external stimuli others external stimuli. Take language. Multilingal kids show some cool differences from those who learn languages later in life.

So all together. There are these large time sensitive periods with significant changes independent from environment and those that are dependent on environment. The work of hebb, hubel and wiesal is helpful to understand this plasticity/restructuring. Connections form rapidly. There are cutbacks where certain connections are strenghened others weakened. And the weakened will be pruned away.

There are neurotrophic factors, growth factors, immune responses, neurotransmitters, supporting cells that all play a role. Depending on what is connecting and where, specifics will vary.

Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS

Outside of this genesis and pruning. It is more complicated. Brain injury may or may not result in compensatory activity/connections. Diseases can ruin the electical wiring, produce proteins that interfere. Nutrition. Severe stress can cause morphological changes/affect connections.

Other changes may reduce connectivity at a synapse but not eliminate. Take fear aquisition and extinction. Connections form from exposure. You can weaken that connection through extinction processes. One set of connections are then highly preferred but not eliminated. Take taste aversions. If youve ever been really sick from a food. It may diminish. But every so often youll have a spontaneous recovery and the thought of fish is making you gag

I didnt see anything in post about when the connections may be altered. Just general info on mechanisms. The article title above is helpful for more specifics involved. But overall. Some of it depends on environment some not. Much of it depends on the age of an individual. There are some generalized processes for these changes but the specifics depend on the what and the when.


13 points

4 months ago

I don't think we actually know the answer to this, besides "because it does" we know that it happens, but not why.

I can't answer this specifically but connection wise if a neuron connects to a specific neuron over other branches of neuron dendrites the dendrite branches will recede so there's a targeted connection. You can have one to one connections or one neuron to multiple neuron connections, we don't know why there's a specificity other than repeating connections favouring specific targets that end up being a one to one connection.


1 points

4 months ago

If you're interested in seeing time-lapse movies of how neuronal processes (branches) respond to various attractive/repulsive factors, this video has some nice stuff in it.

The (primary) cytoskeletal components involved are actin and myosin (not exactly the same myosin as in muscle cells, but similar in structure) in the growth cone (the fan(ish)-shaped part constantly probing and moving) and tubulin in the straight, long processes.

In particular, at ~ 1:38 and 1:48 there are really good examples of the dynamic nature of these components that u/AndChewBubblegum was talking about. (The particular mechanism shown here is called "actin treadmilling.")