Regular spiking in high-conductance states: The essential role of inhibition

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00541638" target="_blank" >RIV/67985823:_____/21:00541638 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/21:10427399

Výsledek na webu

<a href="https://doi.org/10.1103/PhysRevE.103.022408" target="_blank" >https://doi.org/10.1103/PhysRevE.103.022408</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1103/PhysRevE.103.022408" target="_blank" >10.1103/PhysRevE.103.022408</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Regular spiking in high-conductance states: The essential role of inhibition

Popis výsledku v původním jazyce

Strong inhibitory input to neurons, which occurs in balanced states of neural networks, increases synaptic current fluctuations. This has led to the assumption that inhibition contributes to the high spike-firing irregularity observed in vivo. We used single compartment neuronal models with time-correlated (due to synaptic filtering) and state-dependent (due to reversal potentials) input to demonstrate that inhibitory input acts to decrease membrane potential fluctuations, a result that cannot be achieved with simplified neural input models. To clarify the effects on spike-firing regularity, we used models with different spike-firing adaptation mechanisms, and we observed that the addition of inhibition increased firing regularity in models with dynamic firing thresholds and decreased firing regularity if spike-firing adaptation was implemented through ionic currents or not at all. This fluctuation-stabilization mechanism provides an alternative perspective on the importance of strong inhibitory inputs observed in balanced states of neural networks, and it highlights the key roles of biologically plausible inputs and specific adaptation mechanisms in neuronal modeling.

Název v anglickém jazyce

Regular spiking in high-conductance states: The essential role of inhibition

Popis výsledku anglicky

Strong inhibitory input to neurons, which occurs in balanced states of neural networks, increases synaptic current fluctuations. This has led to the assumption that inhibition contributes to the high spike-firing irregularity observed in vivo. We used single compartment neuronal models with time-correlated (due to synaptic filtering) and state-dependent (due to reversal potentials) input to demonstrate that inhibitory input acts to decrease membrane potential fluctuations, a result that cannot be achieved with simplified neural input models. To clarify the effects on spike-firing regularity, we used models with different spike-firing adaptation mechanisms, and we observed that the addition of inhibition increased firing regularity in models with dynamic firing thresholds and decreased firing regularity if spike-firing adaptation was implemented through ionic currents or not at all. This fluctuation-stabilization mechanism provides an alternative perspective on the importance of strong inhibitory inputs observed in balanced states of neural networks, and it highlights the key roles of biologically plausible inputs and specific adaptation mechanisms in neuronal modeling.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10602 - Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology

Projekt

<a href="/cs/project/GA20-10251S" target="_blank" >GA20-10251S: Optimalita neuronální komunikace: informačně-teoretický pohled</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physical Review E

ISSN

2470-0045

e-ISSN

2470-0053

Svazek periodika

103

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

022408

Kód UT WoS článku

000619236600004

EID výsledku v databázi Scopus

2-s2.0-85101275184