An Information Storage Mechanism: Calcium and Spines
This proposal addresses some of the biophysical events possibly underlying fast activity-dependent changes in synaptic efficiency. Dendritic spines in the cortex have attracted increased attention over the last years as a possible locus of cellular plasticity given the large number of studies reporting a close correlation between presynaptic activity (or lack of thereof) and changes in spine shape. This is highlighted by recent reports, showing that the spine cytoplasm contains high levels of actin. Moreover, it has been demonstrated that a high level of intracellular free calcium Ca squared positive, is a prerequisite for various forms of synaptic potentiation. We propose a series of plausible steps, linking presynaptic electrical activity at dendritic spines with a short lasting change in spine geometry. Specifically, we conjecture that the spike-induced excitatory postsynaptic potential triggers an influx of Ca squared positive into the spine, where it will rapidly bind to intracellular calcium buffers such as calmodulin and calcineurin. However, for prolonged or intense presynaptic electrical activity, these buffers will saturate, the free Ca squared positive will then activate the actin/myosin network in the spine neck, reversibly shortening the length of the neck and increasing its diameter. This change in the geometry of the spine will lead to an increase in the synaptic efficiency of the synapse. We will discuss the implication of our proposal for the control of cellular plasticity and its relation to generalized attention and arousal.