The application of a gene to young birds that is closely linked to autism spectrum disorder (ASD) prevents the birds from creating memories necessary to re-create their fathers ’songs. properly represented, a new study led by UT Southwestern shows.
The findings, published online today in Advances in science, may help explain the speech and language deficits that are often associated with ASD and may lead to new treatments that focus specifically on this aspect of the disorder. .
Study director Todd Roberts, Ph.D., associate professor of neuroscience and member of the Brain Institute Peter O’Donnell Jr. at UT Southwestern, explaining that the sounds that are a central part of human communication are virtually unique among the animal world. – not just for their complexity, but in the way they are passed on from carers to children.
Songbirds like zebra knives also learn complex voices from caregivers (songs are usually passed on to males from their fathers).
Just like humans, these animals have a complex brain circulation that is brought to this function, which is found in an area of the brain in birds that is often called the high vocal center, or HVC.
Because of the similarities between language learning in humans and song-learning in birds, Roberts says, songbirds are often used as a scientific model for understanding speech development in humans, introduce situations where voice communication has changed.
In their research, Roberts and his colleagues used zebra finches to study the location of a gene called FoxP1, one of the genes most closely associated with ASD. Mutations of this gene cause a distinct subtype of autism associated with severe language impairment and intellectual disability.
Roberts, a scholar of Thomas O. Hicks in Medical Research, explains that there are two different steps in learning voices for songbirds and humans: First, birds and humans need to remember. on sounds. Next, they use the sounds through recitation.
Juvenile zebra glasses typically use their fathers ’song thousands of times a day over three months, running it around 100,000 times until it’s close. These birds remember the song 20 to 60 days after birth, but do not begin to sing it until about 35 to 40 days after it is born.
To better understand the role FoxP1 who may play a role in all parts of this process, the researchers separated young zebra terminations into two groups: Half of the birds spent their early lives in contact with their singing fathers and continued to sing. stay with them while they used the song; the other half spent their lives early with their mothers without a song and later joined their fathers during rehearsals.
Either before the birds created memories of the songs or before they began to work, Roberts and his colleagues used a method called RNA intervention to “knock down” FoxP1 in the HVC of birds, encephalular cells in this brain region make up the majority of the protein products of this gene.
This approach used structures created in the laboratory of Roberts’ close collaborator and study co-author Genevieve Konopka, Ph.D., associate professor of neuro-science at UT Southwestern.
When the researchers analyzed the birds’ songs in adulthood, they found that only those with active FoxP1 at the time of the song remembrance they were able to reproduce their fathers’ songs correctly.
If this gene were depleted at the practice stage, these birds could still imitate the songs properly. However, birds in which FoxP1 it was put into action before a memoir recalled gloomy songs that were not at all like those sung by their fathers.
“Our results suggest that FoxP1 crucial for creating song memories in those birds that are crucial for later recitation in life, “Roberts says.” Equal deficits in humans may play a parallel role. in speech development, preventing babies from creating memories of adult speech that they hear around them. and hinder their own communication as they grow. “
If this finding is confirmed in future studies, he adds, it could lead to new forms of treatment for children with autism. Conventional ASD treatments based on speech development often aim to help children develop the motor skills necessary to produce sounds.
However, Roberts says, approaches aimed at helping children create verbal memories may be more important. In the future, he says, it may be possible to avoid speech deficits by replacing the required FoxP1 protein by using gene editing or altering FoxP1-regulated signals. use of medicines.
This study is not only necessary for understanding the symptoms of patients with FoxP1Associated ASD but also lays the foundation for the study of many other ASD-related genes using the avian system. “
Genevieve Konopka, PhD, Research Co-author and Associate Professor of Neuroscience, Jon Heighten Scholar in Autism Research, University of Southwestern Texas Medical Center
Source:
Southwestern Texas University Medical Center