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A diffusion-activation model of CaMKII translocation waves in dendrites
Berton A Earnshaw1, Paul C Bressloff
1Department of Mathematics, University of Utah, Salt Lake City, UT 84112-0090, USA.
Journal of Computational Neuroscience
|November 6, 2009
Summary
Calcium-calmodulin-dependent protein kinase II (CaMKII) translocation in dendrites forms a wave. This mathematical model explains CaMKII wave propagation and speed based on diffusion and activation dynamics.
Area of Science:
- Neuroscience
- Molecular Biology
- Computational Biology
Background:
- Ca2+-calmodulin-dependent protein kinase II (CaMKII) regulates glutamatergic synapses.
- CaMKII is crucial for synaptic plasticity.
- Local CaMKII translocation into spines has been observed to spread distally along dendrites.
Purpose of the Study:
- To develop a mathematical model for dendritic CaMKII diffusion, activation, and translocation.
- To elucidate the mechanisms generating CaMKII translocation waves.
- To provide a quantitative framework for understanding CaMKII spread and its role in plasticity.
Main Methods:
- Mathematical modeling of CaMKII dynamics.
- Analysis of nonlinear diffusion-activation dynamics.
- Derivation of a formula for wave speed based on physiological parameters.
Main Results:
- Nonlinear dynamics of CaMKII diffusion-activation can generate propagating translocation waves.
- Wave propagation requires sufficiently fast activation rates.
- An explicit formula for wave speed was derived, dependent on CaMKII diffusivity and spine density.
Conclusions:
- The model quantitatively explains the wave-like spread of CaMKII translocation.
- This mechanism offers insights into CaMKII's role in synaptic plasticity, including heterosynaptic plasticity.
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