Bruker
Products & Solutions
Applications
Services
News & Events
About
Careers
Fluorescence Microscopy Journal Club

Restoring auditory cortex plasticity in adult mice by restricting thalamic adenosine signaling

by Blundon JA, Roy NC1, Teubner BJW, Yu J, Eom TY, Sample KJ, Pani A, Smeyne RJ, Han SB, Kerekes RA, Rose DC, Hackett TA, Vuppala PK, Freeman BB 3rd, Zakharenko SS

Science 2017, 356, pp. 1352-1356

Circuits in the auditory cortex are highly susceptible to acoustic influences during an early postnatal critical period. The auditory cortex selectively expands neuronal representations of enriched acoustic stimuli, a process important for human language acquisition. Adults lack this plasticity. Blundon, Roy at al. demonstrate that with pharmacological intervention, the brain’s cortical plasticity in adult mice could be restored to an extent that is normally seen only in juveniles.

Specifically, the researchers exposed mice to repeated stimulation with pure-tone sound for more than 5 days, while simultaneously rendering the A1R (adenosine A1 receptor) signaling thus reducing presynaptic release of glutamate to the cortex. Reduction of neurotransmitter release led to proportional increase in the cortical area. This effect could be achieved only if A1R signaling was suppressed in the auditory thalamus but not in the cortex. To verify that cortical map plasticity could also be detected on individual neurons, the authors measured tone-evoked activity in individual cortical neurons over time, using a genetically encoded sensor of calcium transients. Suppression of A1R signaling in thalamocortical neurons led to an overall shift in proportion of neurons responding preferentially to the target frequency.

The fact that cortical map plasticity could be induced in adult animals by suppressing A1R signaling suggests that this is a mechanism that is related to the demarcation of the critical period for map plasticity.

The findings should spur research into noninvasive therapies to treat conditions relating to perceptual deficits.