Georgios Kalantzis

Harel Z Shouval

Naveed Aslam

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Spatiotemporal dynamics of calcium and calmodulin at the spine

BioMed CentralBMC Neuroscience
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Spatiotemporal dynamics of calcium and calmodulin at the spine
Georgios Kalantzis1, Naveed Aslam1 and Harel Z Shouval*1,2,3
Address: 1Department of Neurobiology and Anatomy, The University of Texas Medical School, Houston, Texas, USA, 2Department of Biomedical 
Engineering, The University of Texas, Austin, Texas, USA and 3Institute for Brain and Neural Systems, Brown University, Providence, Rhode Island, 
USA
Email: Harel Z Shouval* - harel.shouval@uth.tmc.edu
* Corresponding author    
Calcium levels in spines play a significant role in deter-
mining the sign and magnitude of synaptic plasticity.
Recent experiments using calcium sensitive dyes have
allowed measurements of calcium transients in whole
spines, however experimental resolution does not allow
imaging of the spatial distribution of calcium within the
spine [1,2,5]. Calcium can activate Calcineurin or bind to
CaM and consequently activate CaMKII which is key
mediator of synaptic plasticity. A main source of calcium
influx into the spine is from the NMDA receptors. There
are four different subtypes of obligatory NR2 subunits of
NMDA receptors, NR2A/B/C/D. In the mature cortex the
majority of the synaptic NMDA receptors are constituted
by NR1/NR2A and in the immature cortex by NR1/NR2B.
Experiments have shown that the subunit composition of
NMDA receptors has an influence on the sign of synaptic
plasticity, but different experiments resulted in different
and possibly conflicting results [3,4]. NR2B has slower
kinetics and higher affinity for Glutamate than that of
NR2A. In addition NR2B receptors have a binding site for
CaMKII.
For the study of the spatiotemporal dynamics of Calcium
and Calmodulin we implemented a compartmental
model of the spine head including the neck. We also sim-
ulated an intrinsic calcium buffer and calcium pumps on
the surface of the spine. Calcium pumps and as well as
NMDA receptors were simulated by Markov models [7].
Using this model we observe the spatiotemporal distribu-
tion of calcium and calcium-calmodulin transients. We
find that the calcium pumps as well as the geometry of the
neck affects the spatiotemporal dynamics of calcium and
consequently of calmodulin, and that different NMDA
receptor subunits differentially affect this distribution.
Finally, in the past it has been shown that stochasticity of
calcium transients can affect plasticity rules [6]. We
hypothesize that the main source of stochasticity of cal-
cium transients at the spine arises from the stochasticity of
NMDA receptor opening and presynaptic release. We
investigate the validity of our hypothesis using a stochas-
tic model for the spine. In that way we compare the cal-
cium and calmodulin dynamics of the stochastic model
with those of deterministic and hybrid models.
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from Sixteenth Annual Computational Neuroscience Meeting: CNS*2007
Toronto, Canada. 7–12 July 2007
Published: 6 July 2007
BMC Neuroscience 2007, 8(Suppl 2):P92 doi:10.1186/1471-2202-8-S2-P92
<supplement> <title> <p>Sixteenth Annual Computational Neuroscience Meeting: CNS*2007</p> </title> <editor>William R Holmes</editor> <note>Meeting abstracts – A single PDF containing all abstracts in this Supplement is available <a href="http:www.biomedcentral.com/content/pdf/1471-2202-8-S2-full.pdf">here</a></note> <url>http://www.biomedcentral.com/content/pdf/1471-2202-8-S2-info.pdf</url> </supplement>
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specific gating controls rat NR1/NR2A and NR1/NR2B
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Spatiotemporal dynamics of calcium and calmodulin at the spine

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