Tweaking brain circuits may cure autism

In a ray of hope for people suffering from autism, researchers have discovered neuron populations in a region of the mouse brain that controls whether the animal engages in social behaviour or asocial repetitive self-grooming behaviour.

Autism has also been linked to dysfunction of the amygdala, a brain structure involved in processing emotions. Humans with autism often show a reduced frequency of social interactions and an increased tendency to engage in repetitive solitary behaviour.

Lead researcher David J. Anderson, a Biology professor at the California Institute of Technology and his colleagues discovered two intermingled but distinct population of neurons in the amygdala.

One "social neurons" population promotes social behaviour such as mating, fighting or social grooming while the other "self-grooming neurons" population controls repetitive self-grooming - an asocial behaviour.

To study the relationship between these two cell types and their associated behaviour, researchers used a technique called optogenetics.

Anderson's team was able to selectively switch on the neurons associated with social behaviour and those linked with asocial behaviour.

"Surprisingly, these two groups of neurons appear to interfere with each other's function: the activation of 'social neurons' inhibits self-grooming behaviour while the activation of 'self-grooming neurons' inhibits social behaviour," Anderson noted.

In autism, there is a decrease in social interactions and there is often an increase in repetitive, sometimes asocial or self-oriented behaviour - a phenomenon known as perseveration.

"By stimulating a particular set of neurons, we are both inhibiting social interactions and promoting these persistent behaviours," Anderson said.

If we find the right population of neurons, it might be possible to override the genetic component of a behavioural disorder like autism by just changing the activity of the brain circuits, concluded the study that was reported in the journal Cell.