On the Structure of Ictal Events in Vitro

Traub, Roger D.; Borck, Cornelius; Colling, Simon B.; Jefferys, John G. R.

doi:10.1111/j.1528-1157.1996.tb00042.x

Cited by 156 publications

(109 citation statements)

References 107 publications

(26 reference statements)

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“…To segregate ictal from interictal discharges, we applied the k-means clustering algorithm with squared euclidean distances on the duration of all recorded events and a cutoff at 3 s was chosen to segregate ictal and interictal events. These values are similar to those "arbitrarily" chosen by Traub et al (1996). The duration of both ictal and interictal discharges were defined as the time between the first deflections of the discharge from baseline to its return to baseline.…”

Section: Methodsmentioning

confidence: 78%

KCC2 function modulates in vitro ictogenesis

Hamidi

Avoli

2015

Neurobiology of Disease

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GABA A receptor-mediated inhibition is active and may contribute to epileptiform synchronization. The efficacy of inhibition relies on low levels of intracellular Cl − , which are controlled by KCC2 activity. This evidence has led us to analyze with field potential recordings the effects induced by the KCC2 blockers VU0240551 (10 μM) or bumetanide (50 μM) and by the KCC2 enhancer CLP257 (100 μM) on the epileptiform discharges generated by piriform and entorhinal cortices (PC and EC, respectively) in an in vitro brain slice preparation. Ictal-and interictal-like discharges along with high-frequency oscillations (HFOs, ripples: 80-200 Hz, fast ripples: 250-500 Hz) were recorded from these two regions during application of 4-aminopyridine (4AP, 50 μM). Blocking KCC2 activity with either VU024055 or high doses of bumetanide abolished ictal discharge in both PC and EC; in addition, these experimental procedures decreased the interval of occurrence and duration of interictal discharges. In contrast, enhancing KCC2 activity with CLP257 increased ictal discharge duration in both regions. Finally, blocking KCC2 activity decreased the duration and amplitude of pharmacologically isolated synchronous GABAergic events whereas enhancing KCC2 activity led to an increase in their duration. Our data demonstrate that in vitro ictogenesis is abolished or facilitated by inhibiting or enhancing KCC2 activity, respectively. We propose that these effects may result from the reduction of GABA A receptor-dependent increases in extracellular K + that are known to rest on KCC2 function.

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Section: Methodsmentioning

confidence: 78%

KCC2 function modulates in vitro ictogenesis

Hamidi

Avoli

2015

Neurobiology of Disease

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“…These findings indicate that GABA A receptor-mediated receptor activation actively contributes to sustained prolonged period of epileptiform synchronization. In line with this view, Traub et al (1996) modeled the contribution of GABA A receptor-mediated mechanisms to epileptiform synchronization induced by 4AP, and proposed that depolarizing GABA A receptor-mediated conductances modulate secondary, non-NMDA receptor-dependent bursts in CA3 networks (cf., Avoli et al, 1993). However, both the experimental and the modeling findings obtained from the 4AP model are at variance with those reported by Ziburkus et al (2006) and Derchansky et al (2008) since, as already reviewed in Section 6.1, interneurons recorded during ictal activity appear to be silent due to depolarization block.…”

Section: Mainteinancementioning

confidence: 97%

GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity

Avoli¹,

Curtis²

2011

Progress in Neurobiology

227

253

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GABA is the main inhibitory neurotransmitter in the adult forebrain, where it activates ionotropic type A and metabotropic type B receptors. Early studies have shown that GABA A receptormediated inhibition controls neuronal excitability and thus the occurrence of seizures. However, more complex, and at times unexpected, mechanisms of GABAergic signaling have been identified during epileptiform discharges over the last few years. Here, we will review experimental data that point at the paradoxical role played by GABA A receptor-mediated mechanisms in synchronizing neuronal networks, and in particular those of limbic structures such as the hippocampus, the entorhinal and perirhinal cortices, or the amygdala. After having summarized the fundamental characteristics of GABA A receptor-mediated mechanisms, we will analyze their role in the generation of network oscillations and their contribution to epileptiform synchronization. Whether and how GABA A receptors influence the interaction between limbic networks leading to ictogenesis will be also reviewed. Finally, we will consider the role of altered inhibition in the human epileptic brain along with the ability of GABA A receptor-mediated conductances to generate synchronous depolarizing events that may lead to ictogenesis in human epileptic disorders as well.

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“…For additional quantification of the activity, the data were arbitrarily divided into two categories (cf. Traub et al, 1996): (1) "interictal-type" positive discharges with an interevent interval longer than 3 s, and (2) "ictal-type" synchronous bursts comprising of Ͼ10 discharges, having an interevent interval Ͻ1 s and lasting Ͼ3 s.…”

Section: Methodsmentioning

confidence: 99%

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

Kukko‐Lukjanov

Soini²,

Taira³

et al. 2006

J. Neurosci.

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The central histaminergic neuron system inhibits epileptic seizures, which is suggested to occur mainly through histamine 1 (H 1 ) and histamine 3 (H 3 ) receptors. However, the importance of histaminergic neurons in seizure-induced cell damage is poorly known. In this study, we used an organotypic coculture system and confocal microscopy to examine whether histaminergic neurons, which were verified by immunohistochemistry, have any protective effect on kainic acid (

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On the Structure of Ictal Events in Vitro

Cited by 156 publications

References 107 publications

KCC2 function modulates in vitro ictogenesis

KCC2 function modulates in vitro ictogenesis

GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

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