Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio

Pumain, R.; Ménini, C; Heinemann, Uwe; Louvel, J.; Silva-Barrat, C.

doi:10.1016/0014-4886(85)90280-8

Cited by 120 publications

(67 citation statements)

References 37 publications

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“…Generation and propagation of seizures are generally attributed to spread of activity in excitatory feedback circuits. However, surprisingly "in situ" measurements with ion-selective electrodes show that during seizures, [Ca 2+ ] e drops to levels incompatible with chemical synaptic transmission 47 . Our results may help understand this paradoxical finding and could explain how bursting activity is maintained in absence of chemical synaptic transmission.…”

Section: Implications For Health and Pathologymentioning

confidence: 99%

An astrocyte-dependent mechanism for neuronal rhythmogenesis

et al. 2015

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ABSTRACT:Communication between neurons rests on their capacity to change their firing pattern to encode different messages. For several vital functions, such as respiration and mastication, neurons need to generate a rhythmic firing pattern. Here we show in the rat trigeminal sensori-motor circuit for mastication that this ability depends on regulation of the extracellular Ca 2+ concentration ([Ca 2+ ] e ) by astrocytes. In this circuit, astrocytes respond to sensory stimuli that induce neuronal rhythmic activity, and their blockade with a Ca 2+ chelator prevents neurons from generating a rhythmic bursting pattern.This ability is restored by adding S100β, an astrocytic Ca 2+ -binding protein, to the extracellular space, while application of an anti-S100β antibody prevents generation of rhythmic activity. These results indicate that astrocytes regulate a fundamental neuronal property: the capacity to change firing pattern. These findings may have broad implications for many other neural networks whose functions depend on the generation of rhythmic activity.

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Section: Implications For Health and Pathologymentioning

confidence: 99%

An astrocyte-dependent mechanism for neuronal rhythmogenesis

et al. 2015

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“…The induction of intrinsic bursting by activity-dependent decreases in [Ca 2ϩ ] o also may be germane to the genesis of epileptic seizures. In vivo recordings of [Ca 2ϩ ] o in experimental models of epilepsy have shown dramatic decreases in [Ca 2ϩ ] o (down to 0.2 mM) during seizure activity (Pumain et al, 1985). These decreases would be expected to enhance intrinsic bursting, which in turn would contribute to the explosive development and spread of seizure activity (Jensen and Yaari, 1997).…”

Section: Functional Implicationsmentioning

confidence: 99%

Extracellular Calcium Modulates Persistent Sodium Current-Dependent Burst-Firing in Hippocampal Pyramidal Neurons

Su¹,

Alroy²,

Kirson³

et al. 2001

J. Neurosci.

188

221

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The generation of high-frequency spike bursts ("complex spikes"), either spontaneously or in response to depolarizing stimuli applied to the soma, is a notable feature in intracellular recordings from hippocampal CA1 pyramidal cells (PCs) in vivo. There is compelling evidence that the bursts are intrinsically generated by summation of large spike afterdepolarizations (ADPs). Using intracellular recordings in adult rat hippocampal slices, we show that intrinsic burst-firing in CA1 PCs is strongly dependent on the extracellular concentration of Ca 2ϩ ([Ca 2ϩ

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“…Besides, at the onset of seizures, no matter how induced, [Ca 2+ ] o drops precipitously (Heinemann et al 1977(Heinemann et al , 1978Pumain et al 1983Pumain et al , 1985. Taken together, these two sets of observations suggest that the drop in [Ca 2+ ] o , as also the increase in [K + ] o , may be a link in one of the parallel feedback loops that can promote epileptic seizure discharges.…”

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confidence: 82%

Calcium sensitive non-selective cation current promotes seizure-like discharges and spreading depression in a model neuron

2008

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As described by others, an extracellular calciumsensitive non-selective cation channel ([Ca 2+ ] o -sensitive NSCC) of central neurons opens when extracellular calcium level decreases. An other non-selective current is activated by rising intracellular calcium ([Ca 2+ ] i ). The [Ca 2+ ] osensitive NSCC is not dependent on voltage and while it is permeable by monovalent cations, it is blocked by divalent cations. We tested the hypothesis that activation of this channel can promote seizures and spreading depression (SD). We used a computer model of a neuron surrounded by interstitial space and enveloped in a glia-endothelial "buffer" system. Na + , K + , Ca 2+ and Cl − concentrations, ion fluxes and osmotically driven volume changes were computed. Conventional ion channels and the NSCC were incorporated in the neuron membrane. Activation of NSCC conductance caused the appearance of paroxysmal afterdischarges (ADs) at parameter settings that did not produce AD in the absence of NSCC. The duration of the AD depended on the amplitude of the NSCC. Similarly, NSCC also enabled the generation of SD. We conclude that NSCC can contribute to the generation of epileptiform events and to spreading depression. (Caeser et al. 1993;Crepel et al. 1994) and substantia nigra inhibitory neurons (Lee and Tepper 2007). The TRPM4b channel, which is expressed in mammalian neurons, has been characterized as a [Ca 2+ ] i -activated, Ca 2+ -impermeable, monovalent cation-permeable channel (Fleig and Penner 2004;Launay et al. 2002). Since uptake of Ca 2+ into neurons results simultaneously in an increase in [Ca 2+ ] i and a decrease in [Ca 2+ ] o , if the two Ca 2+ sensitive currents co-exist in the same cell, they are expected to reinforce one another and in fact could perhaps be generated by the same channel (see Section 3).

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Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio

Cited by 120 publications

References 37 publications

An astrocyte-dependent mechanism for neuronal rhythmogenesis

An astrocyte-dependent mechanism for neuronal rhythmogenesis

Extracellular Calcium Modulates Persistent Sodium Current-Dependent Burst-Firing in Hippocampal Pyramidal Neurons

Calcium sensitive non-selective cation current promotes seizure-like discharges and spreading depression in a model neuron

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