An international team of researchers have discovered that a gene critical in the development of human language skills has been shown to help lay down the memories that allow us to perform tasks routinely. Their findings were reported in the Proceedings of the National Academy of Sciences
The FOXP2 gene is the only gene so far confirmed to have a role in speech and language development. While versions exist in many vertebrates, the human version's language function was established through observations of severe speech disorders in people with mutated versions. Intriguingly, songbirds upregulate their FOXP2 genes when changing their tunes. Furthermore, mice without a normal FOXP2 show symptoms associated with autism. FOXP2 also regulates many other genes.
The researchers demonstrated the effects of engineering a human version of the FOXP2 gene into mice.
The human version is only two amino acids different from the normal mouse gene but has previously been shown to encourage synapse development. The gene caused mice to grow longer dendrites, the parts of neurons that communicate with other brain cells, in the striatum. Among the striatium's numerous roles is the development of habits.
The PNAS paper reports mice with the human FOXP2 gene were able to learn more quickly to turn left or right in a T-shaped maze automatically, rather than having to stop and consider their options.
"This really is an important brick in the wall saying that the form of the gene that allowed us to speak may have something to do with a special kind of learning, which takes us from having to make conscious associations in order to act to a nearly automatic-pilot way of acting based on the cues around us," says MIT's Ann Graybiel, one of the professors conducting the research.
The authors found FOXP2 regulates other genes that control the synaptic connections between neurons and enhances dopamine activity in the striatum. In keeping with the maze observations, the human version appears to control mouse neurons in a manner observed when learning new tasks or shifting to procedural memory where we repeat a task we have learned to do by rote. In particular, the altered mice were better at acquiring skills in circumstances where different modes of learning could potentially be in competition.
The authors speculate that the mutation that produced the human version of the FOXP2 gene may have been one of the crucial developments in our acquisition of large brains, both adapting the nervous system for speech and improving our learning capacity.