Humans have far more intelligence and creativity than other animals, and the reason behind this is that humans have extremely strong brains. If we delve more closely into the various brain regions of the human person, we will find that an important source of human intelligence and creativity is the prefrontal cortex and its connection and cooperation with other brain regions.
Decide why you are the brain region of "you."
The prefrontal cortex is located at the front end of the entire frontal lobe of the brain. It regulates people's thoughts and behaviors according to their inner will. Scientists believe that this brain area is closely related to each person's willingness to survive and personality expression.
A more classic example may give us a glimpse into the effects of the prefrontal cortex on humans. In an engineering accident, a thick iron rod destroyed most of the forehead cortex of a railway construction foreman. After the accident, he was originally respected and kind to people, and suddenly became irritable and impulsive, and could no longer communicate with people. In fact, such cases are not uncommon, and scientists have also found that diseases such as autism and schizophrenia are also closely related to prefrontal cortex abnormalities.
In addition to humans, macaques, mice and other animals have this brain area. In contrast, the human prefrontal cortex is larger, has more neurons, and has functional areas that other animals do not have. These characteristics can reflect the superiority of the human brain, but from an evolutionary point of view, humans and other animals have stood at the same starting point, what is the underlying change in these phenomena?
In order to uncover the secrets and find a cure for mental illness, yale scientists, in two papers published in Nature, tried to turn the time of human brain development back to the moment when the prefrontal cortex was about to appear, the second trimester, revealing the secret of the development of brain regions that put human intelligence at the top of the animal kingdom and lost humans.
The key role of tretinoin
After 4-5 months of human embryonic development, the first neural tract in the prefrontal cortex of the brain begins to appear, and then neurons begin to form rapidly in large numbers to form a complete prefrontal cortex. Based on existing brain cell atlas data, the researchers found that the compound retinoic acid has a key regulatory role in neuronal formation, whether in human, macaque, or mouse embryos. Tretinoin is a metabolite of vitamin A in the human body. Previous studies have confirmed that this compound plays a key role in cell proliferation, differentiation, and organ formation.
They found that at least 5 genes in the human brain during this period were regulated by tretinoin, one of which was CBLN2, a gene that promotes synaptic formation and functional realization. By sequencing RNA from the neocortex (including the prefrontal cortex) of humans and macaque monkeys, they found that in the prefrontal cortex of humans and macaques, CBLN2 expression levels were 1.9 times and 2 times that of other brain regions, respectively. In addition, some genes similar to CBLN2, which also promote neuronal development, also have higher expression levels in the prefrontal cortex.
Curiously, however, from the surface of the prefrontal cortex of the human brain to deeper regions, the concentration of tretinoin shows a gradual, more gentle decline, that is, the expression level of the CBLN2 gene gradually decreases from the outside to the inside, but still has a higher expression level in the deepest region of the prefrontal cortex. The concentration of tretinoin in the surface layer of the prefrontal cortex of macaque monkeys is significantly lower than in humans, while in mice, the CBLN2 gene is expressed almost exclusively in the surface layer of the prefrontal cortex. The researchers realized that this seems to be the key to distinguishing the intelligence of the human brain from other animals.
One of the main reasons for this phenomenon is that various animals use different genetic regulation methods. In living organisms, cells will precisely control the expression of genes through certain mechanisms. In this way, the cells can not only ensure the realization of function, but also maximize the saving of resources and energy.
In another study published in Nature, they found a subtle but huge difference in the expression of the CBLN2 gene between humans and other animals. In mice, for example, the expression of the CBLN2 gene is regulated by DNA sequences called enhancers, which bind to proteins or molecules, respectively. When the enhancer binds to tretinoin alone, it enhances gene expression, but when it binds to the SOX5 protein and tretinoin at the same time, the expression of the gene is inhibited. In humans, the sequence binding to the SOX5 protein in the enhancer is directly lost and can only bind to tretinoin, which also means that the CBLN2 gene expression in the human prefrontal cortex is either not expressed or the expression level is very high.
In chimpanzees with higher levels of human and intelligence, the expression of CBLN2 was not suppressed by SOX5, while the expression of the gene in gorillas and macaques was appropriately suppressed. In mice, they have more SOX5 binding sites, and gene expression is strongly inhibited. This small change has a key effect, directly leading to the formation of more dendritic spines on neurons during the development of the person's prefrontal cortex. This allows for more synaptic structures in the prefrontal cortex in the late embryonic development and adulthood, and neurons are more closely linked.
They also found that if human versions of gene sequences such as CBLN2 were introduced into the neurons of mice, the neurons of these mice would indeed form more dendritic spines than normal mice, and the development of deep brain regions in the prefrontal cortex and the connections of other brain regions showed similar characteristics to the brain development process of humans and other primates.
The first dominoes
At the beginning of the embryo becoming a specific person, in the middle of embryonic development, the compound retino acid bulldozed the first domino of prefrontal cortex development. Subsequently, the CBLN2 gene began to be expressed in large quantities, and many dendritic spines formed on the neurons. Dendritic spines in turn promote the formation of synapses that connect different neurons, forming a number of neural circuits that can participate in memory and establish connections with other brain regions. When the frontal cortex is fully developed, tretinoin is degraded by the associated enzymes.
While it is not possible to confirm whether there are genes that affect the development of this brain region, it is certain that tretinoin is critical in the development of the prefrontal cortex. However, the study also leaves some questions: At what time did the primate brain undergo such changes? And how did this change coincidentally remain as a beneficial mutation?
We might guess that the "it" that first had this genetic mutation was the most targeted and intelligent of a primitive population, but because such a brain is more energy-intensive, it is often more likely to feel hungry than other animals in the population. But eventually its genes survived and unexpectedly gave each of its descendants unique characteristics. (According to Global Science)
Source: Science and Technology Daily