Learning language or music is usually a breeze for children, but the capacity declines dramatically with age.
Scientists from St Jude Children's Research Hospital in the US showed that limiting the supply or the function of the neuromodulator adenosine in a brain structure called the auditory thalamus preserved the ability of adult mice to learn from passive exposure to sound much as young children learn from the soundscape of their world.
"By disrupting adenosine signaling in the auditory thalamus, we have extended the window for auditory learning for the longest period yet reported, well into adulthood and far beyond the usual critical period in mice," said Stanislav Zakharenko, a member of the St Jude Department of Developmental Neurobiology.
The auditory thalamus is the brain's relay station where sound is collected and sent to the auditory cortex for processing.
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The auditory thalamus and cortex rely on the neurotransmitter glutamate to communicate.
Adenosine was known to reduce glutamate levels by inhibiting this neurotransmitter's release.
The study, published in the journal Science, linked adenosine inhibition to reduced brain plasticity and the end of efficient auditory learning.
Much as young children pick up language simply by hearing it spoken, researchers showed that when adenosine was reduced or the A1 receptor blocked in the auditory thalamus, adult mice passively exposed to a tone responded to the same tone stronger when it was played weeks or months later.
These adult mice also gained an ability to distinguish between very close tones (or tones with similar frequencies). Mice usually lack this "perfect pitch" ability.
"Taken together, the results demonstrated that the window for effective auditory learning re-opened in the mice and that they retained the information," Zakharenko said.
Among the strategies researchers used to inhibit adenosine activity was the experimental compound FR194921, which selectively blocks the A1 receptor.
If paired with sound exposure, the compound rejuvenated auditory learning in adult mice.
"That suggests it might be possible to extend the window in humans by targeting the A1 receptor for drug development," Zakharenko said.
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