Extracellular free calcium and potassium during paroxysmal activity in the cerebral cortex of the cat

Heinemann, Uwe; Lux, H. D.; Gutnick, Michael J.

doi:10.1007/bf00235500

Cited by 466 publications

(246 citation statements)

References 19 publications

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“…According with this possibility, in some brain conditions characterized by increased neuronal activity and in certain pathological states such as seizures, ischemia, and hypoglycemia, Ca 2 + levels within the extracellular fluid of the brain are reduced and could potentially be sensed by CaSR (Heinemann et al, 1977). CaSR displays significant homology with metabotropic glutamate receptors (mGluRs) expressed in the brain (Nakanishi, 1992;Ruat et al, 1995), and it has been shown that some types of mGluRs, including mGluR3 and mGluR5, are activated not only by glutamate but also by extracellular Ca 2 + (Kubo et al, 1998), although the physiological relevance of this Ca 2 + -sensing property remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

et al. 2009

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Calcium sensing receptor (CaSR), isolated for the first time from bovine and human parathyroid, is a G-protein-coupled receptors that has been involved in diverse physiological functions. At present a complete in vivo work on the identification of CaSR mRNA-expressing cells in the adult brain lacks and this investigation was undertaken in order to acquire more information on cell type expressing CaSR mRNA in the rat brain and to analyse for the first time its expression in different experimental models of brain injury.The expression of CaSR mRNAs was found mainly in scattered cells throughout almost all the brain regions. A double labeling analysis showed a colocalization of CaSR mRNA expression in neurons and oligodendrocytes, whereas it was not found expressed both in the microglia and in astrocytes. One week after kainate-induced seizure CaSR was found in the injured CA3 region of the hippocampus and very interestingly it was found upregulated in the neurons of CA1-CA2 and dentate gyrus. Similarly, 1 week following ibotenic acid injection in the hippocampus, CaSR mRNA expression was increased in oligodendrocytes both in the lesioned area and in the contralateral CA1-CA3 pyramidal cell layers and dentate gyrus. One week after needle-induced mechanical lesion an increase of labeled cells expressing CaSR mRNA was observed along the needle track. In conclusion, the present results contribute to extend available data on cell type-expressing CaSR in normal and injured brain and could spur to understand the role of CaSR in repairing processes of brain injury.

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Section: Discussionmentioning

confidence: 99%

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

et al. 2009

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“…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). Thus, the major cellular generators contributing to the broad range of HFO could evolve dynamically as a seizure progresses and cannot be ascribed to a unique source.…”

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

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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“…Increases in [K + ] o are not unexpected during hypersynchronous activity such as that associated with an interictal discharge that is contributed by glutamatergic conductances leading to sustained action potential firing, and they have been well characterized both in in vivo (Heinemann et al, 1977;Krnjevic et al, 1980) and in vitro preparations Avoli et al, 1990). What is surprising in the 4AP model is that similar [K + ] o elevations can be observed concomitant to the glutamatergic-independent interictal discharges generated by neuronal networks during application of ionotropic glutamatergic receptor antagonists (Fig.…”

Section: [K + ] O Elevations and Slow Interictal Events-as Shown Inmentioning

confidence: 99%

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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Extracellular free calcium and potassium during paroxysmal activity in the cerebral cortex of the cat

Cited by 466 publications

References 19 publications

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

Mechanisms of physiological and epileptic HFO generation

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

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