On the lookout for the causes underlying neocortex expansion, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, at the side of colleagues at the University Hospital Carl Gustav Carus Dresden, in the past identified a variety of molecular players. These players generally act cell-intrinsically in the so-called basal progenitors, the stem cells in the developing neocortex with a pivotal role in its expansion. The researchers now outline an extra, novel role of the happiness neurotransmitter serotonin which is known to operate in the mind to mediate satisfaction, self-confidence, and optimism – to act cell-extrinsically as a growth factor for basal progenitors in the developing human, but not mouse, neocortex.
Because of this new operate, placenta-derived serotonin likely contributed to the evolutionary expansion of the human neocortex. The research team of Wieland Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics, who is likely one of the institute’s founding directors, has investigated the reason for the evolutionary expansion of the human neocortex in many studies. A new study from his lab specializes in the role of the neurotransmitter serotonin in this process. Serotonin is incessantly called the happiness neurotransmitter because it transmits messages between nerve cells that contribute to well-being and happiness. On the other hand, a potential role of such neurotransmitters throughout mind development has not yet been explored in detail.
In the developing embryo, the placenta produces serotonin, which then reaches the mind via blood circulation. This is true for humans in addition to mice. Yet, the operate of this placenta-derived serotonin in the developing mind has been unknown. The postdoctoral researcher Lei Xing in the Huttner group had studied neurotransmitters throughout his doctoral work in Canada. When he started his research project in Dresden after that, he was once curious to enquire their role in the developing mind. “I exploited datasets generated by the group up to now and found that the serotonin receptor HTR2A was once expressed in fetal human, but not embryonic mouse, neocortex. Serotonin needs to bind to this receptor so as to activate downstream signaling. I asked myself whether this receptor could be one of the crucial keys to the question of why humans have a bigger mind,” Lei Xing said.
To explore this, the researchers induced the production of the HTR2A receptor in embryonic mouse neocortex. “Indeed, we found that serotonin, by activating this receptor, caused a chain of reactions that resulted in the production of more basal progenitors in the developing mind. More basal progenitors can then increase the production of cortical neurons, which paves the way to a bigger mind,” said Lei Xing. “In conclusion, our study uncovers a novel role of serotonin as a growth factor for basal progenitors in highly developed brains, notably human. Our data implicate serotonin in the expansion of the neocortex throughout development and human evolution,” said Wieland Huttner, who supervised the study.
“Odd signaling of serotonin and a disturbed expression or mutation of its receptor HTR2A have been observed in quite a lot of neurodevelopmental and psychiatric disorders, such as Down syndrome, attention deficit hyperactivity disorder, and autism. Our findings may help give an explanation for how malfunctions of serotonin and its receptor throughout fetal mind development may end up in congenital disorders and may propose novel approaches for therapeutic avenues,” he added.
(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed.)
Follow more stories on Facebook and Twitter