During human evolution, the size of the brain increased, especially in a certain part called the neocortex. The neocortex allows us to talk, dream and think.
In search of the underlying causes of neocortex enlargement, researchers at the Max Planck Institute for Molecular Cell Biology and Genetics in Dresden, along with colleagues at Carl Gustav Carus University Hospital in Dresden, have previously identified a number of molecular factors.
These players usually act intrinsically in the so-called basal progenitors, the stem cells in the developing neocortex with a key role in its expansion.
Researchers report now an additional role of the neurotransmitter of happiness – serotonin, which is known to work in the brain to mediate satisfaction, self-confidence and optimism. Serotonin can act extrinsically as a growth factor for basal progenitors in humans.
How did the study go?
“We have exploited data sets generated by the group in the past and found that the serotonin HTR2A receptor was expressed in human fetuses, but not in embryonic mice. Serotonin must bind to this receptor to activate downstream signaling. I wondered if this receiver could be one of the answers to the question of why people have a bigger brain, ”explained Lei Xing, a scientist in the research team.
To explore this, the researchers induced the production of the HTR2A receptor in the neocortex of mouse embryos.
“Indeed, we found that serotonin, by activating this receptor, caused a chain of reactions that led to the production of several basal progenitors in the developing brain. More basal progenitors can then increase the production of cortical neurons, which paves the way for a larger brain, ”Lei Xing continues.
Significance for the development and evolution of the brain
What does this new role of serotonin as a growth factor for basal progenitors in highly developed brains entail?
Abnormal signaling of serotonin and a disturbed expression or mutation of its HTR2A receptor have been observed in various neurodevelopmental and psychiatric disorders, such as Down syndrome, attention deficit hyperactivity disorder and autism.
The findings may help explain how defects in serotonin and its receptors during fetal brain development can lead to birth defects, suggesting new approaches to therapeutic treatments.