Can we move the brain cortex up and down?

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The discussion centers on the relationship between brain structure, specifically cortical folding (gyrification), and neural signal transmission efficiency. It highlights how the length of axons affects the speed of signal propagation between different brain areas, emphasizing that shorter axons facilitate quicker communication. The conversation explores the implications of altering the brain's gyrification pattern, suggesting that such changes could significantly impact cognitive function and behavior. Participants discuss the evolutionary significance of current gyrification patterns, questioning whether these configurations are essential for normal mental functioning. They also touch on the variability of cortical folding in healthy individuals and how deviations can lead to neurological disorders, such as schizophrenia. The dialogue raises philosophical inquiries about the nature of brain structure and its role in shaping human cognition and behavior.
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Hello people :oldsmile:

I guess that this is quite fantastic question/idea, but perhaps some day it will be possible to do it :oldeyes:

So, in brain we have got the cortex and the axons that leave one certain area in cortex and enter another area: cortico-cortical afferents/efferents. Some certain amount of time is needed to cover this distance and to propagate the signal/information between these two areas (from A to B). When the signal arrives at destination it will be processed and will be sent to another place. This is simple and clear.

But in brain we have a huge amount of neurons and especially synapses. So, the signal goes from area A to area B, but area B can receive many other signals as well from other neurons/nuclei/structures. But the time when certain signal arrives at area B depends on the length of the axon, right? Shorter axon, earlier the signal will arrive there. Longer the axon, later the signal will arrive there. So, brain’s overall performance highly depends on time when the signals arrive at certain areas.

It means that alongside brain’s other characteristics it is very important white matter’s length(es), more precisely ratio between their length(es). Perhaps we do not change neurons’ overall number in brain, but if we change axons’ length (some of them will become longer, some will become shorter) then brain’s overall performance will be drastically altered.

What these axons’ length depends on? It depends where these two areas are located in the brain, more precisely if these areas are located at the visible/upper part of the cortex or are they folded down into grooves. We know that more than two-thirds of this layer is folded into grooves.

Why this latter circumstance is so important?

Let’s imagine two areas in cortex, A1 and B1 and both are located down in grooves and hence they are invisible and they are connected by cortico-cortical connections and signal flows from A1 to B1. Image below:

ინტელექტის ამაღლება მაიმუნში_1.png

Now let’s imagine that these two areas are located on the visible surface of the cortex and they are again connected by cortico-cortical connections and signal flows from A2 to B2. Image below:
ინტელექტის ამაღლება მაიმუნში_2.png

What is the difference between these two situations? The difference is that in the first case the length of the connections is approximately twice less and hence twice less time is needed for transferring the signal.

Now let’s imagine (quite fantastic) situation where the whole cortex is “turned upside down” in the sense that the areas that originally were located on visible parts of the cortex they were sent downwards and they are invisible now, they are inside the grooves. And the areas that were originally invisible they were sent upwards and they are visible now. It means that length(es) of all cortico-cortical connections will be changed, some will become longer, some will become shorter. Therefore, the time needed for sending signals from one certain area to another area will be changed as well. The order of processing virtually all signals will be altered and brain’s whole performance will be very different.

I wonder to know what mechanisms determine which areas in cortex will be visible and which will go down in grooves? Can we artificially change them in monkeys for example? What do you think, their behavior will be really changed? :oldeyes:
 
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What you are talking about is changing the folding pattern of the cortex. Some of the folds are phylogenetically old and probably pretty invariant while others are more recently evolved.

There are mutations and diseases that can modify or eliminate cortical folding. The more extreme ones probably just eliminate large amounts of cortical area. This alone would cause problems. Increasing cortical area is thought to be the evolutionary reason for folds in the first place, in order to increase processing capability.

There are several things that could affect rate signal transfer in your proposed situation.
  • axon length: longer distance takes more time
  • axon diameter: larger diameter axons transmit faster
  • myelination: myelination greatly speeds transmission, apparently it can vary
  • synaptic delay: chemical transmission involves some chemical diffusion steps (of transmitter molecules going across the synapse), this should also be variable due to ongoing processes maintaining synaptic function.
  • cell structure and electrophysiology: can have effects on how much and how fast synaptic signal are processed to a final cell response.
So there are several things that could be tweeked to maintain proper coordination.
The synaptic delays probably exceed any changes in signal delivery due to changes in axon length.

I am guessing that there are larger scale mechanisms within the brain to do any necessary coordinating.
(There is a lot of variation in the details of brain anatomy, yet most seem to work OK.)

Here is the abstract of an article on how gerbils tune synaptic delays in their auditory brainstem (not the cortex, but similar issues):
Neural computation depends on precisely timed synaptic inputs, but the way that the timing of inputs is tuned to match postsynaptic processing requirements is not well understood. Here, we studied the same brainstem sound localization pathway in two species with dissimilar temporal processing requirements. Two factors that limit precise timing are synaptic delay and axonal conduction time. In gerbils, which depend on precise timing for sound localization, synaptic delays in fast conducting axons are stable across activity level, and axon myelination is adapted to minimize conduction delays. In mice, which do not depend on precise timing, these specializations are absent. Our results suggest that both axonal and synaptic properties are optimized to the specific functional requirements of neural computation, advancing our understanding of the mechanisms that optimize neural circuits.
 
You may also find this discussion of a "minimal common brain" interesting,

Evidence for potentials and limitations of brain plasticity using an atlas of functional resectability of WHO grade II gliomas: towards a "minimal common brain"
Tamara Ius, Elsa Angelini, Michel Thiebaut de Schotten, Emmanuel Mandonnet, Hugues Duffau
https://pubmed.ncbi.nlm.nih.gov/21414413/
http://bcblab.com/BCB/Publications_files/Evidence%20for%20potentials%20and%20limitations%20of%20brain%20plasticity%20using%20an%20atlas%20of%20functional%20resectability%20of%20WHO%20grade%20II%20gliomas_Towards%20a%20minimal%20common%20brain.pdf
 
You are asking about gyrification - development of the ridges in the cortex.
https://en.wikipedia.org/wiki/Gyrification

The gyrification index is a way to quantify normality (or not) of brain development by identifying abnormal gyrification. Gyrification is the orderly development of the gyri (the cortex convolutions you are asking about) in the cortex.

Example:Abnormal development is strongly associated with schizophrenia.
Biological Psychiatry
Volume 41, Issue 10, 15 May 1997, Pages 995-999
1-s2.0-S0006322320X00060-cov150h.gif


"Cortical abnormality in schizophrenia: An in vivo application of the gyrification index"
Jennifer J.Kulynych et al

Lissencephaly is completely missing gyri:

https://en.wikipedia.org/wiki/Lissencephaly

So, deviation in the development of the gyri causes very serious problems or death of the newborn.
 
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BillTre said:
axon length: longer distance takes more time

Of course

BillTre said:
axon diameter: larger diameter axons transmit faster

BillTre said:
myelination: myelination greatly speeds transmission, apparently it can vary

BillTre said:
synaptic delay: chemical transmission involves some chemical diffusion steps (of transmitter molecules going across the synapse), this should also be variable due to ongoing processes maintaining synaptic function.

BillTre said:
cell structure and electrophysiology: can have effects on how much and how fast synaptic signal are processed to a final cell response.

Well, let’s do not complicate the whole image and let’s assume that these factors do not change :oldsmile: but what really changes is only gyrification pattern and axons’ length.

BillTre said:
I am guessing that there are larger scale mechanisms within the brain to do any necessary coordinating.
And are they explored?

Neural computation depends on precisely timed synaptic inputs, but the way that the timing of inputs is tuned to match postsynaptic processing requirements is not well understood. Here, we studied the same brainstem sound localization pathway in two species with dissimilar temporal processing requirements. Two factors that limit precise timing are synaptic delay and axonal conduction time. In gerbils, which depend on precise timing for sound localization, synaptic delays in fast conducting axons are stable across activity level, and axon myelination is adapted to minimize conduction delays. In mice, which do not depend on precise timing, these specializations are absent. Our results suggest that both axonal and synaptic properties are optimized to the specific functional requirements of neural computation, advancing our understanding of the mechanisms that optimize neural circuits.

atyy said:
Evidence for potentials and limitations of brain plasticity using an atlas of functional resectability of WHO grade II gliomas: towards a "minimal common brain"
Tamara Ius, Elsa Angelini, Michel Thiebaut de Schotten, Emmanuel Mandonnet, Hugues Duffau
https://pubmed.ncbi.nlm.nih.gov/21414413/
http://bcblab.com/BCB/Publications_files/Evidence%20for%20potentials%20and%20limitations%20of%20brain%20plasticity%20using%20an%20atlas%20of%20functional%20resectability%20of%20WHO%20grade%20II%20gliomas_Towards%20a%20minimal%20common%20brain.pdf
Interesting and very complex :oldsmile:

jim mcnamara said:
So, deviation in the development of the gyri causes very serious problems or death of the newborn.
I will tell you what is one of the most interesting question to me. So, if I understood correctly if we change gyrification pattern (changing axons’ length) then we receive ill brain (schizophrenia or other disease). But how it happened during the evolution that our current gyrification pattern causes our normal (from the psychological point of view) brain and normal mentality? If gyrification pattern would be different we all would be mentally ill/retarded people, right?

So, was it “by accident” that we, primates/human received such brain with exactly such gyrification pattern? I mean that such gyrification pattern is the only possible one that enables normal mentality, normal thinking, normal civilization and etc? If primates had brain with (a bit) different gyrification pattern then their behavior would be also different but unnormal/”crazy”, right? All they would be crazy, but perhaps crazy people would understand each other.

Of course, this is actually philosophical question, but still – very interesting :cool: what caused exactly such gyrification pattern among other numerous ones? Why exactly this? :oldeyes:
 
Eagle9 said:
I will tell you what is one of the most interesting question to me. So, if I understood correctly if we change gyrification pattern (changing axons’ length) then we receive ill brain (schizophrenia or other disease). But how it happened during the evolution that our current gyrification pattern causes our normal (from the psychological point of view) brain and normal mentality? If gyrification pattern would be different we all would be mentally ill/retarded people, right?

In many of the lissencephaly cases, there are many neuron migration defects. So they aren't necessarily cases of changing the sulci and gyri while leaving everything elsr the same.
 
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Eagle9 said:
Well, let’s do not complicate the whole image and let’s assume that these factors do not change :oldsmile: but what really changes is only gyrification pattern and axons’ length.
That would in my view be a bad assumption.

Eagle9 said:
And are they explored?
To some degree, in other situations.

Eagle9 said:
I will tell you what is one of the most interesting question to me. So, if I understood correctly if we change gyrification pattern (changing axons’ length) then we receive ill brain (schizophrenia or other disease). But how it happened during the evolution that our current gyrification pattern causes our normal (from the psychological point of view) brain and normal mentality? If gyrification pattern would be different we all would be mentally ill/retarded people, right?
I agree with @atyy on this. There are lots of other things wrong in these cases.
Also, there is a degree of variability in the patterns of cortical folding in "normal" people, with no obvious effects.
 
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atyy

BillTre


Thanks :oldsmile:

BillTre said:
Also, there is a degree of variability in the patterns of cortical folding in "normal" people, with no obvious effects.

Yes, in minor sulci/fissurae if I remember correctly :oldeyes:
 

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