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: Eighteenth Annual Computational Neuroscience Meeting: CNS*2009

Open Access Poster presentation

Modeling the excitability of the cerebellar Purkinje cell with detailed calcium dynamics

Haroon Anwar1*, 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

For all author emails, please log on.

BMC Neuroscience 2009, 10(Suppl 1):P34  doi:10.1186/1471-2202-10-S1-P34

The electronic version of this article is the complete one and can be found online at:

Published:13 July 2009

© 2009 Anwar et al; licensee BioMed Central Ltd.

Poster presentation

Previous studies have suggested that the activity pattern of a cerebellar Purkinje cells (PC) is significantly controlled by voltage activated Ca2+ channels and Ca2+ activated K+ channels, present mainly on its elaborate dendritic tree [1]. Although the main somatic excitatory drive propagates very weakly into the dendritic tree [2], somehow a significant interaction between somatic and dendritic spiking occurs. Ca2+ entering through P-type channel is thought to be the main source of this excitability modulation, and this Ca2+ influx also activates large conductance (BK) and small conductance (SK) Ca2+ dependent K+ channels [1,3]. This interaction often results in the counter-intuitive computational somatic and dendritic spiking behavior of PCs [4], but nevertheless this important aspect has not been thoroughly investigated in previous computational modeling studies.

In this work, we try to integrate known aspects of Ca2+ dynamics in PC dendrites by building a new model, which would help us understand the consequent computational properties of a PC. Recently, it has been shown that BK channels are in close vicinity of Ca2+ sources as compared to SK channels [5], suggesting that BK channels require a brief large amount (~10–100 μM) of Ca2+ whereas SK channels require a long yet small quantity (~0.1–2 μM) of Ca2+ for the activation. Therefore it might be interesting to see how this spatiotemporal interaction of Ca2+ sources with Ca2+ activated K+ channels takes place in simulation. Due to lack of sufficient experimental data about the interaction between Ca2+ sources and Ca2+ activated channels in PCs, we could only capture temporal interaction by including Ca2+ dynamics with several buffers and pumps [6] in our model. We expect that this will be sufficient to activate the BK and SK channel correctly. In addition to introducing complex Ca2+ dynamics to our model, we also built new kinetic models of the P-type Ca2+ channel and BK channel based on the recent experimental data [7] and gating kinetics with both voltage and Ca2+ dependence [8].

Not only the composition of active ionic mechanisms, the dendritic morphology can also significantly modify the spiking pattern [9]. However, simulation on the detailed reconstructed morphology of a PC dendritic tree is not suitably efficient for parameter tuning to obtain a desired behavior. Therefore, to investigate the morphological significance in firing behaviors, we have built and used an electrotonically accurate reduced morphology of a PC as well as an even simpler three-compartment model comprising of soma, smooth dendrite and spiny dendrite.


  1. 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. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  2. Vetter P, Roth A, Häusser M: Propagation of action potentials in dendrites depends on dendritic morphology.

    J Neurophysiol 2001, 85:926-937. PubMed Abstract | Publisher Full Text OpenURL

  3. Womack MD, Khodakhah K: Somatic and dendritic small-conductance calcium-activated potassium channels regulate the output of cerebellar purkinje neurons.

    J Neurosci 2003, 23:2600-2607. PubMed Abstract | Publisher Full Text OpenURL

  4. Davie JT, Clark BA, Hausser M: The origin of complex spike in cerebellar Purkinje cells.

    J Neurosci 2008, 28:7599-7609. PubMed Abstract | Publisher Full Text OpenURL

  5. Fakler B, Adelman JP: Control of KCa channels by calcium nano/microdomains.

    Neuron 2008, 59:873-881. PubMed Abstract | Publisher Full Text OpenURL

  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. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  7. Sun XP, Yazejian B, Grinnell AD: Electrophysiological properties of BK channels in Xenopus motor nerve terminals.

    J Physiol 2004, 557:207-228. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  8. Moczydlowski E, Latorre R: Gating Kinetics of Ca2+-activated K+ channels from rat muscle incorporated into planar lipid bilayers.

    J Gen Physiol 1983, 82:511-542. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  9. Mainen ZF, Sejnowski TJ: Influence of dendritic structure on firing pattern in model neocortical neurons.

    Nature 1996, 382:363-366. PubMed Abstract | Publisher Full Text OpenURL