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Genetic technique reverses autism's sensory impairment in mice

By Allen Cone
Genetic technique reverses autism's sensory impairment in mice
A genetic technique reverses sensory impairment in mice with symptoms of autism, offering potential treatment for children with the disorder. Photo by PhotoUG/Shutterstock

Sept. 25 (UPI) -- Scientists have developed a genetic technique that reverses sensory impairment in mice with symptoms of autism, offering potential treatment for children with the disorder.

By switching certain neurons in the brain on or off, mice with autism can learn a sensory task as quickly as healthy ones. Researchers published their findings Monday in the journal Nature Neuroscience.

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"The focus in autism has been trying to tackle social impairment," first author Dr. Anubhuti Goel, a postdoctoral researcher in neurology at UCLA, said in a press release. "But if there is a deficit in learning due to being unable to process certain kinds of sensory input, it affects your development. We're trying to identify early brain processes that will impact behaviors in children when they are older."

Perceptions of visual information are critical to all kinds of learning, including the interpretation of social cues. Children with autism avoid eye contact and struggle to understand people's feelings.

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In the study, researchers used mice with a similar mutation in the FMR1 gene found in humans with fragile X syndrome, a genetic condition that is the most commonly inherited cause of autism.

With the mutation, mice share a number of autism symptoms with people with fragile X syndrome, including anxiety, reduced social interaction and hyper sensory stimuli such as texture and sound.

In the study, mice were trained to lick a drop of water in response to a specific visual cue on a screen. Parallel, black-and-white lines slanting a certain way signified the presence of a water drop. There was no water drop in ones slanted a different way. If the mice took too long to decide, the water drop disappeared.

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Control mice mastered the strategy in about three days but the mice with autism typically required five to nine days.

Researchers recorded brain activity in the mice, finding the visual cortex of the fragile X syndrome mice, or FXS mice, had fewer and less finely tuned neurons, which are pyramidal cells. These excitatory neurons, which serve as the "gas pedal" in the brain are responsible for perceiving the orientation of visual information in rodents, monkeys and humans.

Researchers also found reduced activity in the "brake pedal," known as inhibitory neurons, work with pyramidal cells, kicking them into gear and "tuning" them to respond to specific or more general, bits of visual information.

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The scientists then wanted to see if the inhibitory neurons can be kicked in higher gear to stimulate the pyramidal cells.

They used a genetic technique called DREADD, which stands for Designer Receptors Exclusively Activated by Designer Drugs.

The fragile X syndrome was injected into mice with a virus carrying the genes for these special designer receptors. Then when inside the mouse's parvalbumin cells, the virus generates the DREADD receptors. A drug was administered intravenously that reached those receptors and activated the parvalbumin cells.

The mice learned the visual discrimination task as quickly as their healthy counterparts. The designer drug's effects lasted for three to four hours.

"These experiments shed light on the brain circuit problems behind those difficulties in autism, and hint at directions we can pursue for treatment in the future," Goel said.

Researchers next want to determine what happens in the visual discrimination task with sensory distractors, such as flashing lights or loud sounds.

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