Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Seventeenth Annual Computational Neuroscience Meeting: CNS*2008

Open Access Poster presentation

Can calcium ion contribute to morphological plasticity of a spine?

Keiji Nozawa and Kazuhisa Ichikawa*

Author Affiliations

Department of Brain and Bioinformation Science, Kanazawa Institute of Technology, Hakusan, Ishikawa, Japan

For all author emails, please log on.

BMC Neuroscience 2008, 9(Suppl 1):P101  doi:10.1186/1471-2202-9-S1-P101


The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2202/9/S1/P101


Published:11 July 2008

© 2008 Nozawa and Ichikawa; licensee BioMed Central Ltd.

Introduction

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 [1-4]. 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.

Methods

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.

thumbnailFigure 1. Overall reaction scheme (a) and morphologies used in simulations (b).

Results

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.

thumbnailFigure 2. The change in [Ca2+]i by the change in the size of filopodium (left) and a spine (right).

Discussion

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.

thumbnailFigure 3. Hypothetical mechanism triggering morphological plasticity.

References

  1. Maletic-Savatic M, Malinow R, Svoboda K: Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity.

    Science 1999, 283:1923-1927. PubMed Abstract | Publisher Full Text OpenURL

  2. Matsuzaki M, Honkura N, Ellis-Davies GC, Kasai H: Structural basis of long-term potentiation in single dendritic spines.

    Nature 2004, 429:761-766. PubMed Abstract | Publisher Full Text OpenURL

  3. Fukazawa Y, Fukazawa Y, Saitoh Y, Ozawa F, Ohta Y, Mizuno K, Inokuchi K: Hippocampal LTP is accompanied by enhanced F-actin content within the dendritic spine that is essential for late LTP maintenance in vivo.

    Neuron 2003, 38:447-460. PubMed Abstract | Publisher Full Text OpenURL

  4. Okamoto K, Nagai T, Miyawaki A, Hayashi Y: Rapid and persistent modulation of actin dynamics regulates postsynaptic reorganization underlying bidirectional plasticity.

    Nat Neurosci 2004, 7:1104-1112. PubMed Abstract | Publisher Full Text OpenURL

  5. Ichikawa K: A Modeling Environment with Three-Dimensional Morphology, A-Cell-3D, and Ca2+ Dynamics in a Spine.

    Neuroinformatics 2005, 3:49-64. PubMed Abstract | Publisher Full Text OpenURL

  6. Ichikawa K: A-Cell: graphical user interface for the construction of biochemical reaction models.

    Bioinformatics 2001, 17:483-484. PubMed Abstract | Publisher Full Text OpenURL