ArticlePLoS computational biology2018
Switchable slow cellular conductances determine robustness and tunability of network states.
Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Two-factor synaptic plasticity enables memory consolidation during neuronal burst firing.PNAS nexus · 2026Article
- Burst firing creates an attractor in synaptic weight dynamics.PLoS computational biology · 2026Article
- Quantitative prediction of intracellular dynamics and synaptic currents in a small neural circuit.Frontiers in computational neuroscience · 2025Article
- Robust switches in thalamic network activity require a timescale separation between sodium and T-type calcium channel activations.PLoS computational biology · 2021Article
- Co-opting evo-devo concepts for new insights into mechanisms of behavioural diversity.The Journal of experimental biology · 2019Review
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4 authors.
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Abstract
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 conductance 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 connectivity. 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.
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