Volume 9 Supplement 1

Seventeenth Annual Computational Neuroscience Meeting: CNS*2008

Open Access

Can calcium ion contribute to morphological plasticity of a spine?

BMC Neuroscience20089(Suppl 1):P101

DOI: 10.1186/1471-2202-9-S1-P101

Published: 11 July 2008


Structural plasticity of a spine, which is a change in the spine morphology with synaptic stimulation, has been reported from several labs. Structural plasticity is thought to be a consequence of the induction of long-term potentiation. Some reports suggested the role of actin molecules in the structural plasticity, and the change in F-actin structure will play a pivotal role in the morphological change of a spine [14]. The structure of F-actin is controlled by complex mechanisms, and the molecular mechanisms which contribute to morphological plasticity of a spine are not understood yet. Here, we performed several simulations to see whether the intracellular calcium ion can trigger the structural plasticity of a spine. Simulation results have shown calcium could be a molecule triggering the morphological change of a spine. From these simulation results, we propose a hypothetical mechanism involved in the structural plasticity.


Morphological models including mushroom spines and filopodium with different size in head and neck diameter were constructed using A-Cell software [5, 6]. The 3D morphology was compartmentalized, and Ca2+ entry through NMDA receptors and medium- and low-affinity Ca2+ buffers were embedded to corresponding compartments. Ca2+ diffusion within a spine or filopodum was calculated using Fick's equation. Figure 1 shows the overall reaction schemes and the model morphology.
Figure 1

Overall reaction scheme (a) and morphologies used in simulations (b).


First we simulated the change in the concentration of intracellular calcium ion ([Ca2+]i) in filopodia. The peak [Ca2+]i was increased as the length of filopodium was increased as was expected (Fig. 2 left). However, it was saturated at the filopodium length longer than 1 μm and kept almost the same level. Next, the diameter of a spine head was changed with fixed length of spine neck. With the increase in the spine head diameter, the peak [Ca2+]i was decreased as was expected (Fig. 2 right). However, [Ca2+]i reached a minimum and it kept almost the same level even if the diameter was increased further.
Figure 2

The change in [Ca2+]i by the change in the size of filopodium (left) and a spine (right).


The present simulation results have shown the change in [Ca2+]i with a change in the size of a filopodium and a spine. This suggests that [Ca2+]i can be a triggering molecule for the structural plasticity. The hypothetical mechanism is shown in Figure 3. First, calcium concentration in a localized region of a dendrite is increased forming a 'hot spot'. Second, actin polymerization begins at the 'hot spot' and the protrusion develops increasing the peak [Ca2+]i at its tip. Third, this increase in [Ca2+]i results in further actin polymerization and its bundling. Fourth, protrusion develops further and the peak [Ca2+]i increased. At some level of [Ca2+]i (threshold level), the actin structure at the tip of filopodium is changed from bundling to a meshwork forming a spine head.
Figure 3

Hypothetical mechanism triggering morphological plasticity.

Authors’ Affiliations

Department of Brain and Bioinformation Science, Kanazawa Institute of Technology


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© Nozawa and Ichikawa; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.