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Arc restores juvenile plasticity in adult mouse visual cortex
Kyle R Jenks1, Taekeun Kim2, Elissa D Pastuzyn1
1Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT 84112.
Summary
Augmenting Arc protein in adult mice restores juvenile-like neural plasticity in the visual cortex. This finding offers a molecular explanation for age-related declines in synaptic plasticity.
Area of Science:
- Neuroscience
- Molecular Biology
- Developmental Biology
Background:
- Experience-dependent neural plasticity declines with age.
- Arc, an activity-dependent regulator, is crucial for plasticity during the critical period.
Purpose of the Study:
- To investigate the role of Arc protein in age-related decline of neural plasticity.
- To determine if augmenting Arc expression can restore juvenile-like plasticity in adult mice.
Main Methods:
- Genetic manipulation to augment Arc expression in adult mice.
- In vivo electrophysiological recordings of ocular dominance plasticity.
- Assessing long-term depression (LTD) mechanisms.
Main Results:
- Augmenting Arc expression in adult mice prolonged juvenile-like plasticity.
- Increased LTD was observed in adult mice with augmented Arc.
- Impaired LTD was found in Arc-deficient or protein synthesis-inhibited juvenile mice.
- Arc protein expression declines with age, though mRNA levels remain stable.
Conclusions:
- Arc protein levels are critical for maintaining neural plasticity into adulthood.
- Restoring Arc expression in adult mice can reverse age-related plasticity loss.
- Findings suggest a unifying molecular mechanism for age- and activity-dependent synaptic plasticity.
