Fast activity at seizure onset is mediated by inhibitory circuits in the entorhinal cortex in vitro

Gnatkovsky, Vadym; Librizzi, Laura; Trombin, Federica; Curtis, Marco de

doi:10.1002/ana.21519

Cited by 190 publications

(237 citation statements)

References 61 publications

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“…Here we show they are restricted to electrodes sampling the seizure onset zone. Similar field potentials of larger amplitude precede ictal events in several in vitro models of epilepsy 6,14,[33][34][35] . Moreover, intracranial recordings show PID-like events preceding seizures in multiple focal human epilepsies originating in temporal 17 or extra temporal 36 ; hippocampal 17,18 or neocortical 37 regions, and associated with sclerosis 17,38 , malformation 39 , dysplasia or in macroscopically normal tissue 36 .…”

Section: Discussionmentioning

confidence: 87%

“…3). Excitatory field events similar to PID have been detected just before seizures in animal models 6,8,15,43,44 . PID do not involve barrages of hyperpolarizing synaptic events which may act as an inhibitory restraint, to protect against the spread of seizure-like activities 45 .…”

Section: Discussionmentioning

confidence: 94%

“…In vitro data suggests that interictal events are generated in the CA3 region while seizures may emerge from the entorhinal cortex 5,6 . Interictal population bursts depend on functionally excitatory signaling 5,7 .…”

Section: Introductionmentioning

confidence: 99%

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Glutamatergic pre-ictal discharges emerge at the transition to seizure in human epilepsy

et al. 2011

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Mechanisms involved in the transition to an epileptic seizure remain unclear. We studied this question in tissue slices from human subjects with mesial temporal lobe epilepsies. Ictal-like discharges were induced in the subiculum by increasing excitability together with an alkalinization or low Mg 2+ . During the transition, distinct pre-ictal discharges emerged concurrently with interictal events. Intracranial recordings from the mesial temporal cortex of epileptic subjects revealed similar discharges before seizures were restricted to seizure onset sites. In vitro, pre-ictal events spread faster, have a larger amplitude and a distinct initiation site than interictal discharges. They depend on glutamatergic mechanisms and are preceded by pyramidal cell firing, while interneuron firing precedes interictal events which depend on both glutamatergic and depolarizing GABAergic transmission. Once established, recurrence of these pre-ictal discharges triggers seizures. Thus the subiculum supports seizure generation and the transition to seizure involves a novel, emergent glutamatergic population activity.3

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 94%

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Glutamatergic pre-ictal discharges emerge at the transition to seizure in human epilepsy

et al. 2011

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“…During the progressive recruitment to a seizure, before GABAergic inhibition weakens and an ever growing excitatory drive starts to dominate the firing dynamics (Dzhala and Staley, 2003;Huberfeld et al, 2011;Jiruska et al, 2010a;Timofeev and Steriade, 2004;Trevelyan et al, 2006), there is a major contribution of synchronous GABAergic potentials to HFO in the beta (20-30 Hz) and the gamma range (40-120 Hz) (Gnatkovsky et al, 2008;Köhling et al, 2000;Trevelyan et al, 2006;Trevelyan, 2009). Later on, this rhythmic GABAergic inhibition progressively decreases driven by the collapse of chloride gradients together with a desychronization of interneuronal firing (Derchansky et al, 2008;Dzhala et al, 2010;Gnatkovsky et al, 2008;Lasztoczi et al, 2009;Timofeev et al, 2002b;Viitanen et al, 2010).…”

Section: Single Cell Dynamics During a Wide Range Of Hfo In Epileptogmentioning

confidence: 99%

“…Later on, this rhythmic GABAergic inhibition progressively decreases driven by the collapse of chloride gradients together with a desychronization of interneuronal firing (Derchansky et al, 2008;Dzhala et al, 2010;Gnatkovsky et al, 2008;Lasztoczi et al, 2009;Timofeev et al, 2002b;Viitanen et al, 2010). Then, the local EEG is dominated by large changes in extracellular potassium and calcium that contribute to sustained potentials and slow down oscillatory activity (Amzica et al, 2002;Heinemann et al, 1977;Kaila et al, 1997).…”

Section: Single Cell Dynamics During a Wide Range Of Hfo In Epileptogmentioning

confidence: 99%

Mechanisms of physiological and epileptic HFO generation

Jefferys

Prida

Wendling

et al. 2012

Progress in Neurobiology

268

238

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High frequency oscillations (HFO) have a variety of characteristics: band-limited or broad-band, transient burst-like phenomenon or steady-state. HFOs may be encountered under physiological or under pathological conditions (pHFO). Here we review the underlying mechanisms of oscillations, at the level of cells and networks, investigated in a variety of experimental in vitro and in vivo models. Diverse mechanisms are described, from intrinsic membrane oscillations to network processes involving different types of synaptic interactions, gap junctions and ephaptic coupling. HFOs with similar frequency ranges can differ considerably in their physiological mechanisms. The fact that in most cases the combination of intrinsic neuronal membrane oscillations and synaptic circuits are necessary to sustain network oscillations is emphasized. Evidence for pathological HFOs, particularly fast ripples, in experimental models of epilepsy and in human epileptic patients is scrutinized. The underlying mechanisms of fast ripples are examined both in the light of animal observations, in vivo and in vitro, and in epileptic patients, with emphasis on single cell dynamics. Experimental observations and computational modeling have led to hypotheses for these mechanisms, several of which are considered here, namely the role of out-ofphase firing in neuronal clusters, the importance of strong excitatory AMPA-synaptic currents and recurrent inhibitory connectivity in combination with the fast time scales of IPSPs, ephaptic coupling and the contribution of interneuronal coupling through gap junctions. The statistical behaviour of fast ripple events can provide useful information on the underlying mechanism and can help to further improve classification of the diverse forms of HFOs.

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Seizure‐induced brain‐borne inflammation sustains seizure recurrence and blood–brain barrier damage

Librizzi

Noè

Vezzani

et al. 2012

Annals of Neurology

224

157

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Fast activity at seizure onset is mediated by inhibitory circuits in the entorhinal cortex in vitro

Cited by 190 publications

References 61 publications

Glutamatergic pre-ictal discharges emerge at the transition to seizure in human epilepsy

Glutamatergic pre-ictal discharges emerge at the transition to seizure in human epilepsy

Mechanisms of physiological and epileptic HFO generation

Seizure‐induced brain‐borne inflammation sustains seizure recurrence and blood–brain barrier damage

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