Volume 11 Supplement 1

Nineteenth Annual Computational Neuroscience Meeting: CNS*2010

Open Access

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

BMC Neuroscience201011(Suppl 1):P154

DOI: 10.1186/1471-2202-11-S1-P154

Published: 20 July 2010

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.

Authors’ Affiliations

(1)
Computational Neuroscience Unit, Okinawa Institute of Science and Technology
(2)
Theoretical Neurobiology, University of Antwerp

References

  1. Llinás R, Sugimori M: Electrophysiological properties of in vitro Purkinje cell dendrites in mammalian cerebellar slices. J Physiol (Lond). 1980, 305: 197-213.View ArticleGoogle Scholar
  2. Womack M, Khodakhah K: Active contribution of dendrites to the tonic and trimodal patterns of activity in cerebellar Purkinje neurons. J Neurosci. 2002, 22: 10603-10612.PubMedGoogle Scholar
  3. Edgerton JR, Reinhart PH: Distinct contributions of small and large conductance Ca2+-activated K+ channels to rat Purkinje neuron function. J Physiol. 2003, 548: 53-69. 10.1113/jphysiol.2002.027854.PubMed CentralView ArticlePubMedGoogle Scholar
  4. De Schutter E, Bower JM: Simulated responses of cerebellar Purkinje cells are independent of the dendritic location of granule cell synaptic inputs. Proc Natl Acad Sci U S A. 1994, 91: 4736-4740. 10.1073/pnas.91.11.4736.PubMed CentralView ArticlePubMedGoogle Scholar
  5. Maeda H, Ellis-Davies GC, Ito K, Miyashita Y, Kasai H: Supralinear Ca2+ signaling by cooperative and mobile Ca2+ buffering in Purkinje neurons. Neuron. 1999, 24: 989-1002. 10.1016/S0896-6273(00)81045-4.View ArticlePubMedGoogle Scholar
  6. Schmidt H, Stiefel KM, Racay P, Schwaller B, Eilers J: Mutational analysis of dendritic Ca2+ kinetics in rodent Purkinje cells: role of parvalbumin and calbindin D28k. J Physiol. 2003, 551: 13-32. 10.1113/jphysiol.2002.035824.PubMed CentralView ArticlePubMedGoogle Scholar
  7. Anwar H, Hong S, DeSchutter E: Modeling the excitability of the cerebellar Purkinje cell with detailed calcium dynamics. BMC Neuroscience. 2009, 10: 34-10.1186/1471-2202-10-S1-P34.View ArticleGoogle Scholar

Copyright

© Hong et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.

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