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This article is part of the supplement: Nineteenth Annual Computational Neuroscience Meeting: CNS*2010

Open Access Poster Presentation

Generating dendritic Ca2+ spikes with different models of Ca2+ buffering in cerebellar Purkinje cells

Haroon Anwar12, Sungho Hong1* and Erik De Schutter12

Author Affiliations

1 Computational Neuroscience Unit, Okinawa Institute of Science and Technology, Okinawa 904-0411, Japan

2 Theoretical Neurobiology, University of Antwerp, B-2610 Antwerpen, Belgium

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BMC Neuroscience 2010, 11(Suppl 1):P154  doi:10.1186/1471-2202-11-S1-P154

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2202/11/S1/P154


Published:20 July 2010

© 2010 Hong et al; licensee BioMed Central Ltd.

Poster Presentation

Ca2+ mechanisms, present mainly on the dendritic tree of cerebellar Purkinje cells (PC) [1], significantly influence its activity pattern [2,3], synaptic integration [4], etc. Particularly, the intracellular dynamics controlling Ca2+concentrations can play a crucial role in the physiological interaction between the Ca2+ channels and Ca2+-activated K+ (KCa) channels [5]. The simplest, but commonly used model, the Ca2+ pool with a short relaxation time, will fail to simulate interactions occurring at multiple time scales. On the other hand, detailed computational models including various Ca2+ buffers and pumps [6] can result in large computational cost due to radial diffusion in large compartments, which may need to be avoided when simulating morphologically detailed PC models.

We present a method using compensating mechanisms to replace radial diffusion and compared the dynamics of different Ca2+ buffering models during generation of dendritic Ca2+ spikes during somatic bursting or depolarization [1]. As for the membrane mechanisms, we used a recently constructed single compartment model of a PC dendritic segment with the Ca2+ channels of P- and T-type and KCa channels of BK- and SK-type, which can generate the Ca2+ spikes comparable to the experimental recordings [7]. The Ca2+ dynamics models are (i) a single Ca2+ pool, (ii) two Ca2+ pools respectively for the fast and slow transients, (iii) detailed Ca2+ dynamics with calbindin, parvalbumin, pump and diffusion, and (iv) detailed Ca2+ dynamics with calbindin, parvalbumin, pump and diffusion compensation [6]. The simulated membrane voltage was compared with electrophysiological data.

Our results show that detailed Ca2+ dynamics models with buffers, pumps, and diffusion have significantly better control over Ca2+ activated K+ channels and lead to physiologically more realistic simulations of Ca2+ spikes. Furthermore, the effect on Ca2+ dynamics of removing diffusion from the model can largely be eliminated by the compensating mechanisms. Therefore, physiologically realistic Ca2+ concentration dynamics can be simulated at reasonable computational cost.

References

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