Synchronization of GABAergic Inputs to CA3 Pyramidal Cells Precedes Seizure-Like Event Onset in Juvenile Rat Hippocampal Slices

Lasztóczi, Bálint; Nyitrai, Gabriella; Héja, László; Kardos, Julianna

doi:10.1152/jn.91318.2008

Cited by 49 publications

(41 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…Hence, synaptic inhibition is operative in these in vitro models of interictal discharge. Interestingly, enhanced synchronization of GABAergic inputs to CA3 neurons was demonstrated just ahead of seizures in juvenile rat hippocampal slices bathed in low-magnesium medium (Lasztocki et al, 2009). The changes induced by intracellular injections of hyperpolarizing current on the amplitude of the fast interictal events recorded from pyramidal cells during application of 4AP are indicative of the participation of synaptic currents (Fig.…”

Section: Fast Ca3-driven Interictal Activitymentioning

confidence: 99%

“…18). According to one view (Avoli et al, , 1996aLopantsev and Avoli, 1998a;Fujiwara-Tsukamoto et al, 2004;Gnatkowsky et al, 2008;Lasztocki et al, 2009), interneuronal activity is enhanced and synchronized in the period that precedes a seizure (continuous line). This reduces the firing of principal neurons at seizure onset.…”

Section: Conclusive Remarksmentioning

confidence: 99%

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

Avoli¹,

Curtis²

2011

Progress in Neurobiology

224

253

View full text Add to dashboard Cite

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.

show abstract

“…In these in vitro models, low-voltage fast activity onset is characterized at the start by a prominent activation of inhibitory interneurons (Velazquez and Carlen 1999;Kohling et al 2000;Ziburkus et al 2006;Lasztoczi et al 2009;Fujiwara-Tsukamoto et al 2010), which transiently shut off principal cells ( Fig. 2A) (Gnatkovsky et al 2008).…”

Section: Seizure Onsetmentioning

confidence: 99%

“…Hypersynchronous pattern at seizure onset is most consistently observed when cortical excitability is enhanced in brain slices by a solution containing low magnesium and high potassium (Derchansky et al 2006;Lasztoczi et al 2009;Zhang et al 2012). In these conditions, a gradual recruitment of both inhibitory and excitatory networks occurs (Derchansky et al 2008).…”

Section: Seizure Onsetmentioning

confidence: 99%

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Curtis

Avoli

2015

Cold Spring Harb Perspect Med

View full text Add to dashboard Cite

The neurophysiological patterns that correlate with partial (focal) seizures are well defined in humans by standard electroencephalogram (EEG) and presurgical depth electrode recordings. Seizure patterns with similar features are reproduced in animal models of partial seizures and epilepsy. However, the network determinants that support interictal spikes, as well as the initiation, progression, and termination of seizures, are still elusive. Recent findings show that inhibitory networks are prominently involved at the onset of these seizures, and that extracellular changes in potassium contribute to initiate and sustain seizure progression. The end of a partial seizure correlates with an increase in network synchronization, which possibly involves both excitatory and inhibitory mechanisms.

show abstract

Synchronization of GABAergic Inputs to CA3 Pyramidal Cells Precedes Seizure-Like Event Onset in Juvenile Rat Hippocampal Slices

Cited by 49 publications

References 69 publications

Mechanisms of physiological and epileptic HFO generation

Mechanisms of physiological and epileptic HFO generation

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

Initiation, Propagation, and Termination of Partial (Focal) Seizures

Contact Info

Product

Resources

About