The father of world neuroscience, the Spaniard Santiago Ramón y Cajal, invented precious metaphors to divulge what he himself discovered at the end of the 19th century with his microscope, in animals or in the corpses of children.
Cajal wrote that neurons, the main cells of the brain, were "the mysterious butterflies of the soul", which communicated with each other through "kisses".
More than a century later, the neuroscientist Óscar Marín puts figures in poetry: 100,000 million neurons in each skull, with an average of 1,000 connections each.
It's an inconceivable amount of butterfly kisses.
The human brain is so complex that it is unable to imagine itself.
Marín, born in Madrid 51 years ago, directs the Center for Neurodevelopmental Disorders at King's College London.
On July 15 he will enter the Royal Society of the United Kingdom, a highly reputable institution founded in 1660 to which geniuses such as the naturalist Charles Darwin, the physicist Albert Einstein, the neurologist Rita Levi-Montalcini and Cajal himself belonged.
Marín's discoveries have illuminated the functioning of the cerebral cortex, that gray substance in which the most human characteristics, such as imagination and thought, are concentrated.
His dream goal is to reveal the causes of "some of the most devastating psychiatric disorders, such as autism and schizophrenia."
Ask.
English artist Stephen Wiltshire, diagnosed with autism and wise man syndrome, flew over Madrid by helicopter in 2008 and later drew the entire city from memory.
What happens in those brains?
Response.
The correct answer is that I don't know.
The development of an organ as complex as our brain allows this range of variability.
There is a recipe for generating brains and there are many deviations from it that are compatible with life.
In some cases they produce brains that we recognize as pathological and in other cases, like this one, brains that acquire these super-capabilities.
My intuition, and this is completely speculative, is that these brains are not very different from neurotypical brains [without autism spectrum disorders], but they have acquired some kind of capacity during development, in this case the capacity to fix patterns of form. very stiff.
P.
There are other people with wise man syndrome who listen to a song once and can already play it by heart.
A.
Yes, it is perfect pitch, that ability to recreate musical notes without any problem.
I think that cerebral cortex is not very different from yours or mine.
It's really fascinating that our genome encodes such an enormous variability of behaviors, just by varying little pieces of that incredible puzzle of our cerebral cortex.
From changes in no more than a few dozen genes, a practically identical structure is generated from the morphological point of view, but with a superhero capacity, so to speak.
There is a general idea that the brain is like a computer and parts can be replaced, but in brain development nothing works like that
Q.
You have been elected a member of the Royal Society for your discoveries on the migrations and connections of neurons in the cerebral cortex, especially the inhibitory ones.
A.
Yes, there are two types of neurons, excitatory and inhibitory, which are like yin and yang.
There has to be a very precise balance for the cerebral cortex to work.
It was assumed that all these neurons were born in the same place, that they were formed
in situ,
but we discovered that the inhibitory neurons are not born where the majority of the neurons of the cortex, which are the excitatory ones, but are born in another region of the embryonic brain and migrate a very long distance to reach the crust.
Q.
How long is this trip?
R.
In humans they take weeks to reach their final destination.
In other words, the cortex has a kind of population of resident cells —the autochthonous ones of the cerebral cortex, so to speak, which are the excitatory ones— and a very large population of inhibitory cells that immigrate and end up colonizing this area.
There are approximately four excitatory neurons for each inhibitory one.
Most of the computation is done by the pyramidal cells, which are the excitatory cells.
The inhibitors are like an orchestra conductor: they are in charge of controlling the flow of information between the pyramidal cells, which would be the instruments.
They coordinate that they sound when they should sound and also control their volume: the amount of information they transmit.
When the inhibitors don't work, there is uncontrolled activity in the cortex and epilepsy.
P.
And that conductor arrives migrating from outside the cortex.
A.
Exactly
Q.
It's like the Venezuelan director Gustavo Dudamel.
Q.
Like Dudamel in the Los Angeles Philharmonic, indeed.
It is a very nice way to generate a new structure in the brain.
You have two structures that are working independently, and suddenly, from a mutation, one population of cells becomes migratory and joins the other structure.
And that creates opportunities in the way of managing information, opportunities that did not exist when the population was much more homogeneous.
Q.
What kind of opportunities?
A.
It must represent an evolutionary advantage large enough for such a complicated system to have been preserved for millions of years of evolution.
Because, the larger the brain, the longer the distance these neurons have to travel and the greater the probability of error: that the cells do not arrive at their place, that they are not placed well or that they have problems.
So it's a complicated system to understand in terms of efficiency, but this mixture of neuronal types in the cortex must provide a very important evolutionary advantage.
The parallelism is that talent is universal: societies capable of attracting talent from more places are richer and have a greater capacity to generate new things.
P.
That migration of orchestra conductors to the cerebral cortex can also generate problems.
It could be behind some developmental disorders, such as autism and schizophrenia.
R.
Yes, and epilepsy.
Almost anything that fails in the cortex can cause these types of problems.
Conceptually, the most important change since we started in this business 25 years ago has been that we then thought that any mutation that affected the development of the cerebral cortex would have a more or less homogeneous impact.
We now know that because these two populations of neurons have very different origins, they express very different genes.
We now know that there are mutations that will affect the development of excitatory cells, which make up 80% of the neurons in the cortex.
When there is a problem in the development of these cells, it usually manifests itself in a very visible way, such as macrocephalies or microcephalies.
On the contrary,
P.
And what does that imply?
R.
Perhaps the problems are much finer.
Perhaps there are genes that only affect inhibitory neurons and, therefore, create problems in the generation of these cells, in their migration, in their connectivity.
We know more and more about which genes are important in developing these diseases.
What we still do not fully understand is when and in what population of cells this deviation from normal brain development occurs.
There are probably at least 60 types of excitatory neurons and another 60 types of inhibitory neurons in the cerebral cortex.
Q.
The plasticity of the brain is amazing.
R.
It's really fascinating to see how plastic the brain is.
You do very radical experiments, where you alter very important things, and yet the developing brain has the ability to adapt.
There is a widespread idea that the brain is like a computer.
One would understand developmental illness as missing a piece of the computer, so simply putting it back would be enough.
Nothing really works like that in brain development.
When a piece is missing, or in the wrong place, the rest of the brain will reorganize and rewire itself to try and fill that role.
And that is why there are people who walk around without half of the cerebral cortex or without the cerebellum, such spectacular things that in an adult brain would not be compatible with life.
However, if they occur during development,
the brain looks for ways to compensate for those deficits.
That's why I think it's going to be very difficult to understand some of these diseases, in which surely what we observe is the final product of an initial change and subsequent reorganization of the brain.
The 15 Spaniards in the history of the Royal Society
July 15 will be a historic day for Spanish science.
In addition to the neuroscientist Óscar Marín, the geneticist Irene Miguel Aliaga, a 49-year-old from Barcelona, and the immunologist Carola García de Vinuesa, born in Cádiz 52 years ago and raised in Madrid, will join the prestigious Royal Society in London.
Miguel Aliaga, a researcher at Imperial College London, and García de Vinuesa, also from the Francis Crick Institute in London, will be the first Spanish women to join the Royal Society, a scientific society founded in 1660. The three new recruits will join another three current Spanish members: the chemist Avelino Corma and the geneticists Ginés Morata and Antonio García Bellido.
A spokesman for the Royal Society explains that in the archives of the institution there are only nine other Spanish members, seven from the 18th century,
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