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According to new research done with mice, autism is characterized by reduced activity of inhibitory neurons and increased activity of excitatory neurons in the brain, although balance can be restored with low doses of a well-known type of drugs currently used (in much higher doses) to treat anxiety and epileptic seizures. These findings point to a new therapeutic approach to managing autism. These results suggest that existing drugs, called benzodiazepines, could be effective in treating the core deficits of autism.
As well as finding that mice with autistic characteristics had an imbalance between inhibitory and excitatory neurons in their brains, the research team discovered that reducing the effectiveness of inhibitory neurons in normal mice also induced some autism-related deficits in social behavior. Classical benzodiazepine drugs, however, had the opposite effect, as they increased the activity of inhibitory neurons and diminished autistic behaviors.
These results provide evidence that increasing inhibitory neurotransmission is an effective method to improve social interactions, repetitive behaviors and cognitive deficits in a well-established animal model of autism, with some similar behavioral features as human autism. Therapeutic approaches to treat autistic traits in animal studies or clinical trials have mostly been focused on reducing the activity of excitatory neurons, but with minimal success. These recent results suggest that augmenting the activity of opposing, inhibitory neurons could be an effective alternative strategy.