Depolarization Block of Neurons During Maintenance of Electrographic Seizures

Bikson, Marom; Hahn, Philip; Fox, J. E. D.; Jefferys, John G. R.

doi:10.1152/jn.00467.2003

Cited by 111 publications

(100 citation statements)

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“…The importance of PVBCs in seizure propagation has been recently demonstrated [65]. It was also reported that some neurons can enter into depolarization blocks during seizures [66,67]. We have to note however that the fate of dendritic inhibition is different.…”

Section: Generation Of Interictal Spikes: Changes In Cellular and Netmentioning

confidence: 76%

Generation of physiological and pathological high frequency oscillations: the role of perisomatic inhibition in sharp-wave ripple and interictal spike generation

Gulyás

Freund

2015

Current Opinion in Neurobiology

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Section: Generation Of Interictal Spikes: Changes In Cellular and Netmentioning

confidence: 76%

Generation of physiological and pathological high frequency oscillations: the role of perisomatic inhibition in sharp-wave ripple and interictal spike generation

Gulyás

Freund

2015

Current Opinion in Neurobiology

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“…In others, V m hyperpolarized to a pre-anoxic stage after hyperactivity and cells became quiescent. This does not necessarily imply that these neurons recovered from seizure as this can occur as a result of a depolarization block in which seizure can be maintained even in the absence of continuous neuronal firing (Bikson et al, 2003). While co-antagonism of GABA A and GABA B receptors induced paroxysmal depolarizing shift, blocking either GABA A or GABA B receptors alone did not cause catastrophic depolarization.…”

Section: Discussionmentioning

confidence: 99%

Stellate and pyramidal neurons in goldfish telencephalon respond differently to anoxia and GABA receptor inhibition

Hossein-Javaheri¹,

Wilkie²,

Lado

et al. 2016

Journal of Experimental Biology

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With oxygen deprivation, the mammalian brain undergoes hyperactivity and neuronal death while this does not occur in the anoxiatolerant goldfish (Carassius auratus). Anoxic survival of the goldfish may rely on neuromodulatory mechanisms to suppress neuronal hyper-excitability. As γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain, we decided to investigate its potential role in suppressing the electrical activity of goldfish telencephalic neurons. Utilizing whole-cell patch-clamp recording, we recorded the electrical activities of both excitatory ( pyramidal) and inhibitory (stellate) neurons. With anoxia, membrane potential (V m ) depolarized in both cell types from −72.2 mV to −57.7 mV and from −64.5 mV to −46.8 mV in pyramidal and stellate neurons, respectively. While pyramidal cells remained mostly quiescent, action potential frequency (AP f ) of the stellate neurons increased 68-fold. Furthermore, the GABA A receptor reversal potential (E GABA ) was determined using the gramicidin perforated-patch-clamp method and found to be depolarizing in pyramidal (−53.8 mV) and stellate neurons (−42.1 mV). Although GABA was depolarizing, pyramidal neurons remained quiescent as E GABA was below the action potential threshold (−36 mV pyramidal and −38 mV stellate neurons). Inhibition of GABA A receptors with gabazine reversed the anoxiamediated response. While GABA B receptor inhibition alone did not affect the anoxic response, co-antagonism of GABA A and GABA B receptors (gabazine and CGP-55848) led to the generation of seizure-like activities in both neuron types. We conclude that with anoxia, V m depolarizes towards E GABA which increases AP f in stellate neurons and decreases AP f in pyramidal neurons, and that GABA plays an important role in the anoxia tolerance of goldfish brain.

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“…In this situation the prolonged bursts are primarily synchronized on a slow time scale by transient increases in extracellular K + (Bikson et al, 2003b;Yaari et al, 1983) and on a faster time scale by ephaptic or field effect interactions (Frohlich and McCormick, 2010;Jefferys, 1995). The latter occur when the electrical currents generated by neuronal activity cause a transmembrane depolarization sufficient to nudge neighbouring neurons to threshold; this effect is relatively weak (Jefferys, 1981), but under conditions of heightened excitability, such as in low-Ca 2+ media or during epileptic discharges, neurons are close enough to threshold for this effect to impact on spike timing.…”

Section: Acute Models Of Epilepsy-convulsant Drugsand Changes In Extrmentioning

confidence: 99%

Mechanisms of physiological and epileptic HFO generation

Jefferys

Prida

Wendling

et al. 2012

Progress in Neurobiology

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269

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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Depolarization Block of Neurons During Maintenance of Electrographic Seizures

Cited by 111 publications

References 50 publications

Generation of physiological and pathological high frequency oscillations: the role of perisomatic inhibition in sharp-wave ripple and interictal spike generation

Generation of physiological and pathological high frequency oscillations: the role of perisomatic inhibition in sharp-wave ripple and interictal spike generation

Stellate and pyramidal neurons in goldfish telencephalon respond differently to anoxia and GABA receptor inhibition

Mechanisms of physiological and epileptic HFO generation

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