Increasing the level of the chemical neurotransmitter serotonin made mice with autism are more socialized, the scientists write in the journal Nature. Their study suggests that the same approach can be applied on people with autism. They also give an explanation for why antidepressants do not help with autism: they increase the level of serotonin is too slow to be effective.
The researchers used a method of rapid increase of the levels of serotonin in the nucleus accumbens, a brain area that mediates social reward.
“In a certain way the release of serotonin in the nucleus accumbens play a significant role in increasing sociability,” says lead researcher Robert Malenka, Professor of psychiatry and behavioral Sciences at Stanford University in California. “The simple hypothesis is that it encourages social interaction.”
Serotonin and autism
Decades of research have shown that between serotonin and autism have a connection. About 10 years ago, it has led scientists to test antidepressants that increase levels of serotonin by blocking its reabsorption into neurons, as a possible cure for autism. However, several studies antidepressants like fluoxetine (“Prozac”) have been ineffective in reducing the symptoms of autism.
A new study suggests that the drug, which quickly activates serotonin receptors, is a more effective way to treat this condition.
“We have just begun to understand the mechanisms by which the serotonin system can affect social function and repetitive behaviour,” says Professor of psychiatry, Columbia University Jeremy Veenstra-Vanderweele not taking part in the work.
In the 2013 study team Malenky found that another chemical, a neurotransmitter, oxytocin can make mice more sociable, stimulating serotonin release in the nucleus accumbens.
In the new study, they genetically modified some serotonin-producing neurons, adding them to the photosensitive proteins. Illumination of these neurons activates them, causing serotonin release in the target region, the nucleus accumbens.
Mouse periodically sniffing, preening and otherwise interact with each other, while the scientists turned on the laser, illuminating neurons via a cable in the mouse brain. The interaction between the mice increased dramatically. Mouse programmed to respond to light, also showed a greater preference for another mouse object.
This effect is specific to social behavior: the mouse showed no change in the level of activity or anxiety. Off laser returned the mouse to its previous level of sociability.
Team Malenky also manipulated a different set of mice by using light, which inhibited the activity of the same serotonin neurons. Social interest in mice decreased when switched on the lights.
“The most interesting in this study that the authors found specific brain area and specific types of cells that have a causal relationship with the social behavior of animals related to autism,” says Guo-Li Ming, a neuroscientist from the University of Pennsylvania.
The researchers then deleted region of chromosome 16 called 16p11.2 in the same serotonin neurons. (About 1 percent of people with autism not have a copy of this field).
This deletion reduces the activity of neurons. Mice with deletion of neurons spend less time interacting with other mice and did not show preference to another mouse over an object.
Activation of neurons with light immediately makes the mice more social, counteracting the effects of removal. Infusion into the nucleus accumbens of mice a drug that blocks the serotonin receptor, reverses the effect of light, suggesting that serotonin mediates the increase in sociability.
The results “surprising,” but “we need to be careful not to exaggerate their” consequences, says Veenstra-Vanderweele. In particular, according to him, the mice in the study were not both copies of the 16p11.2 in these neurons, while the autistic people among the people with this deletion have only one. Moreover, other commands are not found in mice lacking one copy of this region in all cells, problems with social skills.