Ion channels are a promising target to treat sensory symptoms in autism spectrum disorders

What is it about?

Problems in sensory integration are a frequent symptom of Fragile X syndrome (FXS) and other autism spectrum disorders (ASD). In this study we show that Fragile X mice have defects in the way sensory information is treated by the neocortex – the part of the brain responsible for sensory perception, generation of motor commands, spatial reasoning and conscious thought. We show that the neocortex of these mice is hyperexcited in response to tactile sensory stimuli. We then conducted a range of detailed tests showing that this neocortical hyperexcitability is related to the way neurons in this brain region integrate this information. As a result of this investigation, we found that certain ion channels – molecules that determine the way neurons process electrical signals – are altered in their dendrites (the structures that integrate information and which behave much like the ‘brains’ of neurons). By using a pharmacological agonist of one of these channels, we found that we could correct this neocortical hyperexcitability and neuronal integration defects.

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Why is it important?

Importantly we were able to correct neocortical hyper-excitability and a behavioral readout for sensory hypersensitivity. Normal mice were not affected by this treatment. These findings offer new hope for a tailored treatment for sensory aspects of ASD and FXS - in particular as these treatments could be applied in adolescent or adult patients.