Enhanced nonsynaptic epileptiform activity in the dentate gyrus after kainate-induced status epilepticus

Nogueira, G.S.; Santos, Luiz Eduardo Canton; Rodrigues, Antônio Márcio; Scorza, Carla A.; Scorza, Fúlvio A.; Cavalheiro, Ésper A.; Almeida, Antonio Carlos

doi:10.1016/j.neuroscience.2015.06.057

Cited by 8 publications

(8 citation statements)

References 25 publications

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“…It has been reported that right following KA-induced epilepsy, hippocampal neurons strongly expressed immediate early genes c-Fos and c-Jun, which encode transcription factors (Kim et al, 2008 ). In the brain of KA model, a bunch of neurotransmitters, receptors and ion channels were observed increased including voltage-gated sodium channel Nav1.6 (Zhu et al, 2016 ), Na + /K + /Cl − cotransporter (Nogueira et al, 2015 ), metabotropic glutamate receptors (mGluRs) especially mGluR2/3 (Caulder et al, 2014 ) and mGluR5 (Medina-Ceja and García-Barba, 2017 ), ATP-activated P2Y receptors (Alves et al, 2017 ) and acetylcholine neurotransmission (Soares et al, 2017 ). Besides the activation of these excitatory mechanisms, other mechanisms involved in KA-induced hyperexcitability have also been documented.…”

Section: Discussionmentioning

confidence: 99%

Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Pan

Chen

Zheng

et al. 2018

Front. Neural Circuits

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Epilepsy is one of the most common neurological disorders affecting millions of people. Due to the complicated and unclear mechanisms of epilepsy, still a significant proportion of epilepsy patients remain poorly controlled. Epilepsy is characterized by convulsive seizures that are caused by increased excitability. In this study, by using kainic acid (KA)-induced epilepsy mice, we investigated the neuronal activities and revealed the neuronal compensatory mechanisms after KA-induced toxic hyperexcitability. The results indicate that both phasic inhibition induced by enhanced inhibitory synaptic activity and tonic inhibition mediated by activated astrocytes participate in the compensatory mechanisms. Compensatory mechanisms were already found in various neuronal disorders and were considered important in protecting nervous system from toxic hyperexcitability. This study hopefully will provide valuable clues in understanding the complex neuronal mechanisms of epilepsy, and exploring potential clinical treatment of the disease.

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Section: Discussionmentioning

confidence: 99%

Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Pan

Chen

Zheng

et al. 2018

Front. Neural Circuits

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“…It is hypothesized that an abnormal depolarizing GABAergic function caused by an imbalance in NKCC1 and KCC2, may cause rewiring of excitatory glutamatergic neuronal circuits and play a role in the epileptogenic processes (87). NKCC1 not only plays a key role in facilitating synaptic epileptiform activity, but also in non-synaptic epileptiform activity in the dentate gyrus (91). Increased seizure susceptibility and depolarized E GABA caused by chronic stress may imply an imbalance in chloride homeostasis and can be reversed with bumetanide (92).…”

Section: Dysregulation Of Nkcc1/kcc2 In Epilepsy Changes In Function mentioning

confidence: 99%

Role of NKCC1 and KCC2 in Epilepsy: From Expression to Function

et al. 2020

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As a main inhibitory neurotransmitter in the central nervous system, γ-aminobutyric acid (GABA) activates chloride-permeable GABAa receptors (GABAa Rs) and induces chloride ion (Cl −) flow, which relies on the intracellular chloride concentration ([Cl − ] i) of the postsynaptic neuron. The Na-K-2Cl cotransporter isoform 1 (NKCC1) and the K-Cl cotransporter isoform 2 (KCC2) are two main cation-chloride cotransporters (CCCs) that have been implicated in human epilepsy. NKCC1 and KCC2 reset [Cl − ] i by accumulating and extruding Cl − , respectively. Previous studies have shown that the profile of NKCC1 and KCC2 in neonatal neurons may reappear in mature neurons under some pathophysiological conditions, such as epilepsy. Although increasing studies focusing on the expression of NKCC1 and KCC2 have suggested that impaired chloride plasticity may be closely related to epilepsy, additional neuroelectrophysiological research aimed at studying the functions of NKCC1 and KCC2 are needed to understand the exact mechanism by which they induce epileptogenesis. In this review, we aim to briefly summarize the current researches surrounding the expression and function of NKCC1 and KCC2 in epileptogenesis and its implications on the treatment of epilepsy. We will also explore the potential for NKCC1 and KCC2 to be therapeutic targets for the development of novel antiepileptic drugs.

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“…The non-synaptic influence of neurons to neighbors occurs mainly due to ED. The J o u r n a l P r e -p r o o f ED has been demonstrated to have a strong effect between neurons in the neural tissue (66) and may be a factor for pathological states (14,45,67,68).This finding could be explained by the fact that the ED modulates neuronal excitability and, thus, the type of electrophysiological pattern. However, if all neighboring neurons of the cell assemblies receive the same influence from ED, the ability of the cell assembly to quickly process information vanished.…”

Section: Discussionmentioning

confidence: 99%

Realistic spiking neural network: Non-synaptic mechanisms improve convergence in cell assembly

et al. 2020

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Enhanced nonsynaptic epileptiform activity in the dentate gyrus after kainate-induced status epilepticus

Cited by 8 publications

References 25 publications

Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Compensatory Mechanisms Modulate the Neuronal Excitability in a Kainic Acid-Induced Epilepsy Mouse Model

Role of NKCC1 and KCC2 in Epilepsy: From Expression to Function

Realistic spiking neural network: Non-synaptic mechanisms improve convergence in cell assembly

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