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Generating dendritic Ca2+ spikes with different models of Ca2+ buffering in cerebellar Purkinje cells
BMC Neuroscience volume 11, Article number: P154 (2010)
Ca2+ mechanisms, present mainly on the dendritic tree of cerebellar Purkinje cells (PC) , significantly influence its activity pattern [2, 3], synaptic integration , 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 . 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  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 . 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 . 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 . 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.
Llinás R, Sugimori M: Electrophysiological properties of in vitro Purkinje cell dendrites in mammalian cerebellar slices. J Physiol (Lond). 1980, 305: 197-213.
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.
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.
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.
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.
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.
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.
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Anwar, H., Hong, S. & De Schutter, E. Generating dendritic Ca2+ spikes with different models of Ca2+ buffering in cerebellar Purkinje cells. BMC Neurosci 11, P154 (2010). https://doi.org/10.1186/1471-2202-11-S1-P154
- Purkinje Cell
- Radial Diffusion
- Dendritic Tree
- Cerebellar Purkinje Cell
- Multiple Time Scale