Higher-order thalamic nuclei facilitate the generalization and maintenance of spike-and-wave discharges of absence seizures

Spike-and-wave discharges (SWDs), generated by the cortico-thalamo-cortical (CTC) network, are pathological, large amplitude oscillations and the hallmark of absence seizures (ASs). SWDs begin in a cortical initiation network in both humans and animal models, including the Genetic Absence Epilepsy R...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Atherton Zoe
Nagy Olivér
Barcsai Lívia
Sere Péter
Zsigri Nikolett
Földi Tamás
Gellért Levente
Berényi Antal
Crunelli Vincenzo
Lőrincz László Magor
Dokumentumtípus: Cikk
Megjelent: 2023
Sorozat:NEUROBIOLOGY OF DISEASE 178
Tárgyszavak:
doi:10.1016/j.nbd.2023.106025

mtmt:33789523
Online Access:http://publicatio.bibl.u-szeged.hu/27689
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520 3 |a Spike-and-wave discharges (SWDs), generated by the cortico-thalamo-cortical (CTC) network, are pathological, large amplitude oscillations and the hallmark of absence seizures (ASs). SWDs begin in a cortical initiation network in both humans and animal models, including the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), where it is located in the primary somatosensory cortex (S1). The behavioral manifestation of an AS occurs when SWDs spread from the cortical initiation site to the whole brain, however, the mechanisms behind this rapid propagation remain unclear. Here we investigated these processes beyond the principal CTC network, in higher-order (HO) thalamic nuclei (lateral posterior (LP) and posterior (PO) nuclei) since their diffuse connectivity and known facilitation of intracortical communications make these nuclei key candidates to support SWD generation and maintenance. In freely moving GAERS, multi-site LFP in LP, PO and multiple cortical regions revealed a novel feature of SWDs: during SWDs there are short periods (named SWD-breaks) when cortical regions far from S1, such the primary visual cortex (V1), become transiently unsynchronized from the ongoing EEG rhythm. Inactivation of HO nuclei with local muscimol injections or optogenetic perturbation of HO nuclei activity increased the occurrence of SWD-breaks and the former intervention also increased the SWD propagation-time from S1. The neural underpinnings of these findings were explored further by silicon probe recordings from single units of PO which uncovered two previously unknown groups of excitatory neurons based on their burst firing dynamics at SWD onset. Moreover, a switch from tonic to burst firing at SWD onset was shown to be an important feature since it was much less prominent for non-generalized events, i.e. SWDs that remained local to S1. Additionally, one group of neurons showed a reverse of this switch during SWD-breaks, demonstrating the importance of this firing pattern throughout the SWD. In summary, these results support the view that multiple HO thalamic nuclei are utilized at SWD onset and contribute to cortical synchrony throughout the paroxysmal discharge. 
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700 0 1 |a Nagy Olivér  |e aut 
700 0 1 |a Barcsai Lívia  |e aut 
700 0 1 |a Sere Péter  |e aut 
700 0 1 |a Zsigri Nikolett  |e aut 
700 0 1 |a Földi Tamás  |e aut 
700 0 1 |a Gellért Levente  |e aut 
700 0 1 |a Berényi Antal  |e aut 
700 0 1 |a Crunelli Vincenzo  |e aut 
700 0 1 |a Lőrincz László Magor  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/27689/1/32Athertonetal2023NBD.pdf  |z Dokumentum-elérés