Reference : Switchable slow cellular conductances determine robustness and tunability of network ...
Scientific journals : Article
Engineering, computing & technology : Multidisciplinary, general & others
http://hdl.handle.net/2268/223719
Switchable slow cellular conductances determine robustness and tunability of network states
English
Drion, Guillaume mailto [Université de Liège - ULiège > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Systèmes et modélisation >]
Dethier, Julie mailto [Université de Liège - ULiège > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Systèmes et modélisation >]
Franci, Alessio mailto [Universidad Nacional Autonoma de Mexico > Department of Mathematics >]
Sepulchre, Rodolphe mailto [Université de Liège - ULiège > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Systèmes et modélisation >]
23-Apr-2018
PLoS Computational Biology
Public Library of Science
14
e1006125
Yes (verified by ORBi)
International
1553-734X
1553-7358
CA
[en] Neuromodulation ; brain states ; negative conductance
[en] Neuronal information processing is regulated by fast and localized fluctuations of brain states. Brain states reliably switch between distinct spatiotemporal signatures at a network scale even though they are composed of heterogeneous and variable rhythms at a cellular scale. We investigated the mechanisms of this network control in a conductance-based population model that reliably switches between active and oscillatory mean-fields. Robust control of the mean-field properties relies critically on a switchable negative intrinsic conduc- tance at the cellular level. This conductance endows circuits with a shared cellular positive feedback that can switch population rhythms on and off at a cellular resolution. The switch is largely independent from other intrinsic neuronal properties, network size and synaptic con- nectivity. It is therefore compatible with the temporal variability and spatial heterogeneity induced by slower regulatory functions such as neuromodulation, synaptic plasticity and homeostasis. Strikingly, the required cellular mechanism is available in all cell types that possess T-type calcium channels but unavailable in computational models that neglect the slow kinetics of their activation.
http://hdl.handle.net/2268/223719
10.1371/journal.pcbi.1006125

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