scholarly journals Robust switches in thalamic network activity require a timescale separation between sodium and T-type calcium channel activations

2021 ◽  
Vol 17 (5) ◽  
pp. e1008997
Author(s):  
Kathleen Jacquerie ◽  
Guillaume Drion

Switches in brain states, synaptic plasticity and neuromodulation are fundamental processes in our brain that take place concomitantly across several spatial and timescales. All these processes target neuron intrinsic properties and connectivity to achieve specific physiological goals, raising the question of how they can operate without interfering with each other. Here, we highlight the central importance of a timescale separation in the activation of sodium and T-type calcium channels to sustain robust switches in brain states in thalamic neurons that are compatible with synaptic plasticity and neuromodulation. We quantify the role of this timescale separation by comparing the robustness of rhythms of six published conductance-based models at the cellular, circuit and network levels. We show that robust rhythm generation requires a T-type calcium channel activation whose kinetics are situated between sodium channel activation and T-type calcium channel inactivation in all models despite their quantitative differences.

2020 ◽  
Author(s):  
Kathleen Jacquerie ◽  
Guillaume Drion

AbstractSwitches in brain states, synaptic plasticity and neuromodulation are fundamental processes in our brain that take place concomitantly across several spatial and timescales. All these processes target neuron intrinsic properties and connectivity to achieve specific physiological goals, raising the question of how they can operate without interfering with each other. Here, we highlight the central importance of a timescale separation in the activation of sodium and T-type calcium channels to sustain robust switches in brain states in thalamic neurons that are compatible with synaptic plasticity and neuromodulation. We quantify the role of this timescale separation by comparing the robustness of rhythms of six published conductance-based models at the cellular, circuit and network levels. We show that robust rhythm generation requires a T-type calcium channel activation whose kinetics are situated between sodium channel activation and T-type calcium channel inactivation in all models despite their quantitative differences.


1997 ◽  
Vol 122 (5) ◽  
pp. 949-955 ◽  
Author(s):  
Shiow-Chwen Tsai ◽  
Jiann-Jong Chen ◽  
Yu-Chung Chiao ◽  
Chien-Chen Lu ◽  
Ho Lin ◽  
...  

2003 ◽  
Vol 279 (5) ◽  
pp. 3793-3800 ◽  
Author(s):  
Stephanie C. Stotz ◽  
Wendy Barr ◽  
John E. McRory ◽  
Lina Chen ◽  
Scott E. Jarvis ◽  
...  

1997 ◽  
Vol 272 (6) ◽  
pp. 3560-3566 ◽  
Author(s):  
Nikolai M. Soldatov ◽  
Roger D. Zühlke ◽  
Alexandre Bouron ◽  
Harald Reuter

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Nikolai M. Soldatov

Voltage-gated L-type Cav1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca2+ concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis. Inactivation or spontaneous termination of the calcium current through Cav1.2 is a critical step in regulation of these processes. The pathophysiological significance of this process is manifested in hypertension, heart failure, arrhythmia, and a number of other diseases where acceleration of the calcium current decay should present a benefit function. The central issue of this paper is the inactivation of the Cav1.2 calcium channel mediated by multiple determinants.


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