Bidirectional control of absence seizures by the basal ganglia: a computational evidence.

Absence epilepsy is believed to be associated with the abnormal interactions between the cerebral cortex and thalamus. Besides the direct coupling, anatomical evidence indicates that the cerebral cortex and thalamus also communicate indirectly through an important intermediate bridge-basal ganglia....

Full description

Bibliographic Details
Main Authors: Mingming Chen, Daqing Guo, Tiebin Wang, Wei Jing, Yang Xia, Peng Xu, Cheng Luo, Pedro A Valdes-Sosa, Dezhong Yao
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-03-01
Series:PLoS Computational Biology
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24626189/?tool=EBI
id doaj-cf340ed2d7614992bf8bf6801ecd0744
record_format Article
spelling doaj-cf340ed2d7614992bf8bf6801ecd07442021-04-21T15:36:17ZengPublic Library of Science (PLoS)PLoS Computational Biology1553-734X1553-73582014-03-01103e100349510.1371/journal.pcbi.1003495Bidirectional control of absence seizures by the basal ganglia: a computational evidence.Mingming ChenDaqing GuoTiebin WangWei JingYang XiaPeng XuCheng LuoPedro A Valdes-SosaDezhong YaoAbsence epilepsy is believed to be associated with the abnormal interactions between the cerebral cortex and thalamus. Besides the direct coupling, anatomical evidence indicates that the cerebral cortex and thalamus also communicate indirectly through an important intermediate bridge-basal ganglia. It has been thus postulated that the basal ganglia might play key roles in the modulation of absence seizures, but the relevant biophysical mechanisms are still not completely established. Using a biophysically based model, we demonstrate here that the typical absence seizure activities can be controlled and modulated by the direct GABAergic projections from the substantia nigra pars reticulata (SNr) to either the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of thalamus, through different biophysical mechanisms. Under certain conditions, these two types of seizure control are observed to coexist in the same network. More importantly, due to the competition between the inhibitory SNr-TRN and SNr-SRN pathways, we find that both decreasing and increasing the activation of SNr neurons from the normal level may considerably suppress the generation of spike-and-slow wave discharges in the coexistence region. Overall, these results highlight the bidirectional functional roles of basal ganglia in controlling and modulating absence seizures, and might provide novel insights into the therapeutic treatments of this brain disorder.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24626189/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Mingming Chen
Daqing Guo
Tiebin Wang
Wei Jing
Yang Xia
Peng Xu
Cheng Luo
Pedro A Valdes-Sosa
Dezhong Yao
spellingShingle Mingming Chen
Daqing Guo
Tiebin Wang
Wei Jing
Yang Xia
Peng Xu
Cheng Luo
Pedro A Valdes-Sosa
Dezhong Yao
Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
PLoS Computational Biology
author_facet Mingming Chen
Daqing Guo
Tiebin Wang
Wei Jing
Yang Xia
Peng Xu
Cheng Luo
Pedro A Valdes-Sosa
Dezhong Yao
author_sort Mingming Chen
title Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
title_short Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
title_full Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
title_fullStr Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
title_full_unstemmed Bidirectional control of absence seizures by the basal ganglia: a computational evidence.
title_sort bidirectional control of absence seizures by the basal ganglia: a computational evidence.
publisher Public Library of Science (PLoS)
series PLoS Computational Biology
issn 1553-734X
1553-7358
publishDate 2014-03-01
description Absence epilepsy is believed to be associated with the abnormal interactions between the cerebral cortex and thalamus. Besides the direct coupling, anatomical evidence indicates that the cerebral cortex and thalamus also communicate indirectly through an important intermediate bridge-basal ganglia. It has been thus postulated that the basal ganglia might play key roles in the modulation of absence seizures, but the relevant biophysical mechanisms are still not completely established. Using a biophysically based model, we demonstrate here that the typical absence seizure activities can be controlled and modulated by the direct GABAergic projections from the substantia nigra pars reticulata (SNr) to either the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of thalamus, through different biophysical mechanisms. Under certain conditions, these two types of seizure control are observed to coexist in the same network. More importantly, due to the competition between the inhibitory SNr-TRN and SNr-SRN pathways, we find that both decreasing and increasing the activation of SNr neurons from the normal level may considerably suppress the generation of spike-and-slow wave discharges in the coexistence region. Overall, these results highlight the bidirectional functional roles of basal ganglia in controlling and modulating absence seizures, and might provide novel insights into the therapeutic treatments of this brain disorder.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24626189/?tool=EBI
work_keys_str_mv AT mingmingchen bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT daqingguo bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT tiebinwang bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT weijing bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT yangxia bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT pengxu bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT chengluo bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT pedroavaldessosa bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
AT dezhongyao bidirectionalcontrolofabsenceseizuresbythebasalgangliaacomputationalevidence
_version_ 1714667321792921600