State transitions through inhibitory interneurons in a cortical network model.

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 investi...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Alexander Bryson, Samuel F Berkovic, Steven Petrou, David B Grayden
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2021
Materias:
Acceso en línea:https://doaj.org/article/b1c70c995cf946a084eb9e65c8d6ffe3
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:b1c70c995cf946a084eb9e65c8d6ffe3
record_format dspace
spelling oai:doaj.org-article:b1c70c995cf946a084eb9e65c8d6ffe32021-12-02T19:57:29ZState transitions through inhibitory interneurons in a cortical network model.1553-734X1553-735810.1371/journal.pcbi.1009521https://doaj.org/article/b1c70c995cf946a084eb9e65c8d6ffe32021-10-01T00:00:00Zhttps://doi.org/10.1371/journal.pcbi.1009521https://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358Inhibitory 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.Alexander BrysonSamuel F BerkovicSteven PetrouDavid B GraydenPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 17, Iss 10, p e1009521 (2021)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Alexander Bryson
Samuel F Berkovic
Steven Petrou
David B Grayden
State transitions through inhibitory interneurons in a cortical network model.
description 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.
format article
author Alexander Bryson
Samuel F Berkovic
Steven Petrou
David B Grayden
author_facet Alexander Bryson
Samuel F Berkovic
Steven Petrou
David B Grayden
author_sort Alexander Bryson
title State transitions through inhibitory interneurons in a cortical network model.
title_short State transitions through inhibitory interneurons in a cortical network model.
title_full State transitions through inhibitory interneurons in a cortical network model.
title_fullStr State transitions through inhibitory interneurons in a cortical network model.
title_full_unstemmed State transitions through inhibitory interneurons in a cortical network model.
title_sort state transitions through inhibitory interneurons in a cortical network model.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/b1c70c995cf946a084eb9e65c8d6ffe3
work_keys_str_mv AT alexanderbryson statetransitionsthroughinhibitoryinterneuronsinacorticalnetworkmodel
AT samuelfberkovic statetransitionsthroughinhibitoryinterneuronsinacorticalnetworkmodel
AT stevenpetrou statetransitionsthroughinhibitoryinterneuronsinacorticalnetworkmodel
AT davidbgrayden statetransitionsthroughinhibitoryinterneuronsinacorticalnetworkmodel
_version_ 1718375859899858944