Revisiting an old concept: the coupled oscillator model for VCD. Part 2: implications of the generalised coupled oscillator mechanism for the VCD robustness concept

2016 ◽  
Vol 18 (31) ◽  
pp. 21213-21225 ◽  
Author(s):  
Valentin Paul Nicu

The generalised coupled oscillator (GCO) mechanism implies that the stability of the computed VCD sign should be assigned by monitoring the uncertainties in the relative orientation of the GCO fragments and in the nuclear displacement vectors, i.e. not the magnitude of the dissymmetry factor.

1993 ◽  
Vol 18 (21) ◽  
pp. 1810 ◽  
Author(s):  
Herbert G. Winful ◽  
Sean Allen ◽  
Lutfur Rahman

2006 ◽  
Vol 95 (2) ◽  
pp. 932-947 ◽  
Author(s):  
Alexey S. Kuznetsov ◽  
Nancy J. Kopell ◽  
Charles J. Wilson

Dopaminergic neurons of the midbrain fire spontaneously at rates <10/s and ordinarily will not exceed this range even when driven with somatic current injection. When driven at higher rates, these cells undergo spike failure through depolarization block. During spontaneous bursting of dopaminergic neurons in vivo, bursts related to reward expectation in behaving animals, and bursts generated by dendritic application of N-methyl-d-aspartate (NMDA) agonists, transient firing attains rates well above this range. We suggest a way such high-frequency firing may occur in response to dendritic NMDA receptor activation. We have extended the coupled oscillator model of the dopaminergic neuron, which represents the soma and dendrites as electrically coupled compartments with different natural spiking frequencies, by addition of dendritic AMPA (voltage-independent) or NMDA (voltage-dependent) synaptic conductance. Both soma and dendrites contain a simplified version of the calcium-potassium mechanism known to be the mechanism for slow spontaneous oscillation and background firing in dopaminergic cells. The compartments differ only in diameter, and this difference is responsible for the difference in natural frequencies. We show that because of its voltage dependence, NMDA receptor activation acts to amplify the effect on the soma of the high-frequency oscillation of the dendrites, which is normally too weak to exert a large influence on the overall oscillation frequency of the neuron. During the high-frequency oscillations that result, sodium inactivation in the soma is removed rapidly after each action potential by the hyperpolarizing influence of the dendritic calcium-dependent potassium current, preventing depolarization block of the spike mechanism, and allowing high-frequency spiking.


2019 ◽  
Vol 15 (8) ◽  
pp. e1006575 ◽  
Author(s):  
Gihan Weerasinghe ◽  
Benoit Duchet ◽  
Hayriye Cagnan ◽  
Peter Brown ◽  
Christian Bick ◽  
...  

2007 ◽  
Author(s):  
Jorge A. González ◽  
Jose J. Suárez-Vargas ◽  
Aneta Stefanovska ◽  
Peter V. E. McClintock

2012 ◽  
Vol 194 ◽  
pp. 111-121 ◽  
Author(s):  
Yuichi Ikeda ◽  
Hideaki Aoyama ◽  
Yoshi Fujiwara ◽  
Hiroshi Iyetomi ◽  
Kazuhiko Ogimoto ◽  
...  

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