The capacity of learning is less in adults. Researchers have restricted the chemical adenosine in the brain region to extend auditory learning till adulthood.
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‘Adenosine inhibition not only reduced the efficiency of auditory learning, but also reduced brain plasticity.’
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"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 corresponding author Stanislav Zakharenko, M.D., Ph.D., a member of the St. Jude Department of Developmental Neurobiology.
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"These results offer a promising strategy to extend the same window in humans to acquire language or musical ability by restoring plasticity in critical regions of the brain, possibly by developing drugs that selectively block adenosine activity."
The auditory thalamus is the brain’s relay station where sound is collected and sent to the auditory cortex for processing.
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. This study also linked adenosine inhibition to reduced brain plasticity and the end of efficient auditory learning.
Researchers used a variety of methods to demonstrate that reducing adenosine or blocking the A1 adenosine receptor that is essential to the chemical messenger’s function changed how adult mice responded to sound.
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Researchers also showed that the experimental mice retained the improved tone discrimination for weeks.
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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.
Zakharenko and his colleagues also linked the age-related decline in ease of auditory learning to an age-related increase in an enzyme (ecto-5’-nucleotidase) involved in adenosine production in the auditory thalamus.
Researchers reported that mature mice had higher levels than newborn mice of the enzyme and adenosine in the auditory thalamus. Deletion of this enzyme returned the adenosine level in adult mice to the level of newborn mice. Therefore, researchers are currently looking for compounds that target ecto-5’-nucleotidase as an alternative approach for extending the window of auditory learning.
Source-Eurekalert