Calcium-mediated spine stem restructuring

Abstract

A spine is a protrusion from the dendritic (or somatic) surface of a neuron. In recent experiments, caffeine-induced calcium released from internal stores was shown to cause elongation of dendritic spine stems in slice cultures. Still another experiment indicates that glutamate-induced increases in calcium may cause spine stem shortening. Harris draws a schematic model to explain these seemingly conflicting results, indicating that a small amount of activity may increase free calcium within the spines and cause spine stem elongation, but an excessive amount of activity may increase intraspine calcium beyond a critical level and cause spine stem shortening (see [1, Figure 2]). This paper develops a mathematical model for a fixed population of spines along the dendrite, each with a dynamic structure and calcium level. The system is integrated over time and space to observe an interdependent relationship between calcium, morphology and chemical/electrical activity. Results of simulation qualitatively capture phenomena observed in recent experiments and exhibit periodic oscillations in potential when the spines have excitable membrane properties by allowing spine structure to transition through threshold geometries for generation of action potentials in a bidirectional manner. As in recent experiments, a variety of chemical and structural profiles emerge, depending on membrane properties, patterns of synaptic input, and initial conditions considered.