A popular advertising campaign may wish to convince us that ‘it’s good to talk’, but research into the brain chemicals released during language exchanges suggests the claim is truer than we might think.
Previous studies have shown that a gene known as FoxP2 plays a part in the severe stuttering and stammering suffered by some people. Until recently the mechanism behind its role was not properly understood. Now a study from the Duke University School of Medicine in the US suggests that a defect in the FoxP2 gene makes the brain insensitive to the feel-good chemical dopamine, which is involved in the reinforcement of learned behaviours like singing or playing sports.
It has long been known that the gene is not only found in humans, but is evident among all vertebrates. To get an insight into the gene’s role in speech, Professor Richard Mooney and Dr Malavika Murugan decided to look at its effect on the call of songbirds.
Zebrafinches begin learning how to sing from an early age. They do this by listening to a male tutor and then repeating what they have heard thousands of times a day until they are able to make a very good copy of the song. But it is in the presence of females that a male finch’s song becomes particularly precise, especially when he is directing it to a specific female in courtship.
As part of their investigations of the gene’s role in the songbird’s call, FoxP2 activity was suppressed in the brain of male zebrafinches. These males were then introduced to females and their song recorded in order to discern specific changes in comparison to the song of non-altered birds.
The study, published in the journal Neuron, found that altering the gene did not prevent the ability of the male birds to learn their song. However, when in the presence of a female, their ability to hit the right note was impaired. This is would profoundly affect the likelihood mating.
This finding, that FoxP2 is involved in voice control rather than language learning, had not been possible to make in humans with FOXP2 mutations.
Prof Mooney said: “FoxP2 mutations do not simply result in a cognitive or learning deficit, but also produce an ongoing motor deficit. Individuals with these mutations can still learn and can still improve; it is just harder for them to reliably hit the right mark.”
The area of the brain where the ‘active’ gene is found to be turned on in humans – the basal ganglia – is known to be dysfunctional in the brains of people suffering from Tourette syndrome. This condition is known for its vocal tics and outbursts. The area is also shrunk in individuals with FoxP2 mutations.
Further research showed that the chemical dopamine influences how fast basal ganglia signals propagate in birds with normal FoxP2, but not in those with the mutated gene.
Dr Murugan said: “This switch between undirected and directed song is actually dependent on the influx of this neurotransmitter called dopamine.
“So what we think is happening is knocking down FoxP2 makes the male incapable of reducing song variability in the presence of a female. An adult male sees the female, there is an influx of dopamine, but because the system is insensitive, the dopamine has no effect and the adult male continues to sing a variable tune.”
The authors of the study are at pains to point out that their findings relate to birdsong, and should not be taken as proof of the mechanism in human. But they say their study does highlight the value of songbirds in studying human behaviours and disease.
“Birds are one of the few non-human animals that learn to vocalise,” Dr Mooney said.
“They produce songs for courtship that they culturally transmit from one generation to the next. Their brains might be a thousandth the size of ours, but in this one dimension, vocal learning, they are our equal.”