Neuroscientists at Harvard and MIT have identified, for the first time, a link between the activity of the neurotransmitter GABA and symptoms of autism -- a finding that may pave the way for new methods of treating and diagnosing the disorder.
“This is the first connection in humans between a neurotransmitter in the brain and an autistic behavioral symptom,” Caroline Robertson, a postdoc at MIT’s McGovern Institute for Brain Research and the study's lead author, said in a statement.
The role of the GABA neurotransmitter is to inhibit brain cells from firing in response to signals received from the external environment -- or as Robertson told The Huffington Post, to curb "runaway excitation" in the brain.
"GABA is responsible for signaling that neurons should turn off, or stop firing," Robertson told HuffPost. "It tends to come into play ... when information is being transmitted and it needs to be shut down or filtered out."
Scientists have speculated that a lack of GABA inhibition to overexcited neurons could be the underlying cause of the hypersensitivity to sensory input seen in individuals with autism.
"It's necessary to filter out signals in the external world that aren't relevant to the task at hand," Robertson said. "GABA helps us in this kind of inhibition."
Hypersensitivity to one's external environment makes it difficult for individuals with autism to tune out distracting sounds and sensations, and can make them feel overwhelmed in loud or highly stimulating situations. For instance, some children with autism tend to be easily distracted by sensations like the feel of an itchy sweater or by ambient noise in the background of a conversation. Hypersensitivity also plays a role in the main symptoms of the disorder, including impaired social skills, communication difficulties and repetitive behaviors.
So, it may be that when GABA doesn't do it's job, it's more difficult for the brain to tune out environmental distractions.
Scientists had suspected this, but had never tested the hypothesis on humans. Previous studies had linked reduced GABA activity with autism-like behaviors in animals, but no such correlation had been established in people.
For the study, the researchers asked a group of participants -- half of whom had autism, and half of whom did not -- to complete a visual task that required brain inhibition. Completing the task hinges on the ability to switch between visual input from the right and left eyes.
The results showed that adults with autism switched back and forth only half as much as those without autism, and they were significantly less able to suppress one image in order to focus on the other.
While the participants completed the task, the researchers measured GABA activity in their brains. Among non-autistic participants, those with higher GABA levels were better able to suppress the non-dominant image. But among those with autism, there was no relationship between performance on the task and GABA levels -- suggesting that in the case of autism, GABA is "not doing its job," Robertson said.
"It's not as simple as GABA is missing in the autistic brain," Robertson explained. "It's not in lower concentration, it's just not relating to visual perception."
The researchers aren't yet sure of the cause for this dysfunction. "A lot more work needs to be done," she said.
More research is needed to determine whether increasing GABA activity could improve symptoms of autism, but the findings are a promising start towards improving early diagnosis, treatment and perhaps even prevention of autism. In addition to opening up the possibility of new drugs that target GABA pathways, clinicians might also one day be able to examine GABA activity in early screenings for autism.
"It'll be a longer story than just, Aha! We'll make some GABA-enhancing drugs and cure autism," Robertson said. "But it does point to a pathway that seems to be dysfunctional in the autistic brain."
Other recent brain-imaging studies have found differences in functional connectivity between autistic and non-autistic brains, and have also linked impaired brain activity with the inability to regulate emotions in individuals with autism.
The findings were published online Dec. 17 in the journal Current Biology.