PMC:7160870 / 5152-6098 JSONTXT

{"project":"TEST0","denotations":[{"id":"32100552-229-234-3683","span":{"begin":646,"end":647},"obj":"[\"12769430\"]"}],"text":"But how does this novel appraisal of glial cells’ role sit with our existing models of brain dynamics in epileptic seizures? Decades of theoretical work in epilepsy have focused on how disturbances in the intricate balance between coupled excitatory and inhibitory neuronal populations allow for transitions of brain dynamics into pathological, epileptic regimes. In fact many key features of epileptic seizures—such as their sudden emergence from resting brain activity, the widespread synchronization across brain areas, or the sudden seizure offset—can be explained with simple models of coupled excitatory and inhibitory neuronal populations.6 An example toy model consisting of coupled excitatory and inhibitory populations is shown in Figure 1A. Here the effect of an acute reduction in inhibitory transmission (as could be induced by PTZ) leads to the emergence of synchronized large amplitude oscillations, after a “threshold” is crossed."}

{"project":"MyTest","denotations":[{"id":"32100552-12769430-28640681","span":{"begin":646,"end":648},"obj":"12769430"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"But how does this novel appraisal of glial cells’ role sit with our existing models of brain dynamics in epileptic seizures? Decades of theoretical work in epilepsy have focused on how disturbances in the intricate balance between coupled excitatory and inhibitory neuronal populations allow for transitions of brain dynamics into pathological, epileptic regimes. In fact many key features of epileptic seizures—such as their sudden emergence from resting brain activity, the widespread synchronization across brain areas, or the sudden seizure offset—can be explained with simple models of coupled excitatory and inhibitory neuronal populations.6 An example toy model consisting of coupled excitatory and inhibitory populations is shown in Figure 1A. Here the effect of an acute reduction in inhibitory transmission (as could be induced by PTZ) leads to the emergence of synchronized large amplitude oscillations, after a “threshold” is crossed."}

{"project":"0_colil","denotations":[{"id":"32100552-12769430-3683","span":{"begin":646,"end":647},"obj":"12769430"}],"text":"But how does this novel appraisal of glial cells’ role sit with our existing models of brain dynamics in epileptic seizures? Decades of theoretical work in epilepsy have focused on how disturbances in the intricate balance between coupled excitatory and inhibitory neuronal populations allow for transitions of brain dynamics into pathological, epileptic regimes. In fact many key features of epileptic seizures—such as their sudden emergence from resting brain activity, the widespread synchronization across brain areas, or the sudden seizure offset—can be explained with simple models of coupled excitatory and inhibitory neuronal populations.6 An example toy model consisting of coupled excitatory and inhibitory populations is shown in Figure 1A. Here the effect of an acute reduction in inhibitory transmission (as could be induced by PTZ) leads to the emergence of synchronized large amplitude oscillations, after a “threshold” is crossed."}

{"project":"2_test","denotations":[{"id":"32100552-12769430-28640681","span":{"begin":646,"end":647},"obj":"12769430"}],"text":"But how does this novel appraisal of glial cells’ role sit with our existing models of brain dynamics in epileptic seizures? Decades of theoretical work in epilepsy have focused on how disturbances in the intricate balance between coupled excitatory and inhibitory neuronal populations allow for transitions of brain dynamics into pathological, epileptic regimes. In fact many key features of epileptic seizures—such as their sudden emergence from resting brain activity, the widespread synchronization across brain areas, or the sudden seizure offset—can be explained with simple models of coupled excitatory and inhibitory neuronal populations.6 An example toy model consisting of coupled excitatory and inhibitory populations is shown in Figure 1A. Here the effect of an acute reduction in inhibitory transmission (as could be induced by PTZ) leads to the emergence of synchronized large amplitude oscillations, after a “threshold” is crossed."}

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