Health&Wellness Magazine March 2016 | Page 17

March 2016 & GABA and Autism 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 autism. Harvard University and Massachusetts Institute of Technology (MIT) neuroscientists have identified a link between the activity of the neurotransmitter GABA and symptoms of autism. “This is the first connection in humans between a neurotransmitter in the brain and an autistic behavioral symptom,” said the study’s lead author, Caroline Robertson, a post doc at MIT’s McGovern Institute for Brain Research. The GABA neurotransmitter inhibits brain cells from firing in response to signals received from the external environment to curb “runaway excitation” in the brain, according to Roberts. In other words, GABA tells neurons they should stop firing and turn off. 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 autism. This hypersensitivity is the biggest problem for those with autism. The inability to tune out distracting sounds and sensations make them feel overwhelmed. Hypersensitivity also plays a role in the main symptoms of autism: impaired social skills, communication difficulties and repetitive behaviors. Thus, it seems when GABA doesn’t function properly, it is more difficult for the brain to filter out environmental distractions. Previous studies have linked reduced GABA activity with autism-like behavior in animals, but this is the first study to show the same results in humans. Although the link has been established, it is not known whether increasing GABA activity could improve the symptoms of autism. “It’ll be a longer story than just, ‘Aha! We’ll make some GABA-enhancing drugs and cure autism,’” said Robertson. “But it does point to a pathway that seems to be dysfunctional in the autistic brain.” The findings were published in the Dec. 17 issue of the journal Current Biology. 17