State transitions through inhibitory interneurons in a cortical network model.


Journal

PLoS computational biology
ISSN: 1553-7358
Titre abrégé: PLoS Comput Biol
Pays: United States
ID NLM: 101238922

Informations de publication

Date de publication:
10 2021
Historique:
received: 13 04 2021
accepted: 04 10 2021
revised: 27 10 2021
pubmed: 16 10 2021
medline: 15 12 2021
entrez: 15 10 2021
Statut: epublish

Résumé

Inhibitory interneurons shape the spiking characteristics and computational properties of cortical networks. Interneuron subtypes can precisely regulate cortical function but the roles of interneuron subtypes for promoting different regimes of cortical activity remains unclear. Therefore, we investigated the impact of fast spiking and non-fast spiking interneuron subtypes on cortical activity using a network model with connectivity and synaptic properties constrained by experimental data. We found that network properties were more sensitive to modulation of the fast spiking population, with reductions of fast spiking excitability generating strong spike correlations and network oscillations. Paradoxically, reduced fast spiking excitability produced a reduction of global excitation-inhibition balance and features of an inhibition stabilised network, in which firing rates were driven by the activity of excitatory neurons within the network. Further analysis revealed that the synaptic interactions and biophysical features associated with fast spiking interneurons, in particular their rapid intrinsic response properties and short synaptic latency, enabled this state transition by enhancing gain within the excitatory population. Therefore, fast spiking interneurons may be uniquely positioned to control the strength of recurrent excitatory connectivity and the transition to an inhibition stabilised regime. Overall, our results suggest that interneuron subtypes can exert selective control over excitatory gain allowing for differential modulation of global network state.

Identifiants

pubmed: 34653178
doi: 10.1371/journal.pcbi.1009521
pii: PCOMPBIOL-D-21-00661
pmc: PMC8550371
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1009521

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Alexander Bryson (A)

Ion Channels and Disease Group, The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Australia.
Department of Neurology, Austin Health, Heidelberg, Australia.

Samuel F Berkovic (SF)

Epilepsy Research Centre, Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Australia.

Steven Petrou (S)

Ion Channels and Disease Group, The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Australia.

David B Grayden (DB)

Department of Biomedical Engineering, University of Melbourne, Melbourne, Australia.

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Classifications MeSH