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Activity-dependent increase in beta-amyloid precursor protein mRNA expression in neurons

Akiko Tabuchi1, Asami Ishii, Mamoru Fukuchi

  • 1Department of Biological Chemistry, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Sugitani 2630, Toyama 930-0194, Japan.

Neuroreport
|May 29, 2004
PubMed

Insights

Beta-amyloid precursor protein (APP) mRNA expression in neurons is regulated by neuronal activity. High potassium levels increase APP mRNA, while reduced activity decreases it, highlighting activity-dependent control.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Beta-amyloid precursor protein (APP) is implicated in neuronal survival and plasticity.
  • The regulation of APP mRNA expression by neuronal activity remains largely uncharacterized.

Purpose of the Study:

  • To investigate the relationship between neuronal activity and APP mRNA expression in neurons.
  • To elucidate the mechanisms underlying activity-dependent regulation of APP mRNA.

Main Methods:

  • Primary cultures of mouse cerebellar granule cells were used.
  • Neuronal activity was manipulated by altering extracellular potassium (K+) concentration.
  • APP mRNA and protein levels were quantified.
  • Calcium influx and protein synthesis pathways were examined.

Main Results:

  • High potassium concentrations significantly increased APP mRNA levels.
  • Depolarization-induced K+ deprivation reduced both APP mRNA expression and protein synthesis.
  • Restoring high K+ concentrations restored APP mRNA expression.
  • This regulation was dependent on calcium (Ca2+) influx via L-type voltage-dependent calcium channels and de novo protein synthesis.

Conclusions:

  • APP mRNA expression in neurons is controlled in an activity-dependent manner.
  • Neuronal activity, specifically membrane depolarization, modulates APP gene expression.
  • Calcium signaling pathways are crucial for this activity-dependent regulation of APP.

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