Post-treatment of an NADPH oxidase inhibitor prevents seizure-induced neuronal death

Kim, Jin Hee; Jang, Bong Geom; Choi, Bo Young; Kim, Hyeong Seop; Sohn, Min; Chung, Tae Nyoung; Choi, Hyeong‐Ah; Song, Heesang; Suh, Sang Won

doi:10.1016/j.brainres.2013.01.007

Cited by 64 publications

(60 citation statements)

References 41 publications

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“…* p < 0.05; ** p < 0.01; *** p < 0.001. in vitro and in vivo. These findings are in keeping with our recent in vitro findings (Kovac et al, 2014) and also with recent papers highlighting the role of NADPH oxidase in in vivo models of epilepsy (Pestana et al, 2010;Kim et al, 2013). This also indirectly supports a pivotal role of NMDA receptors in epilepsy, with recent reports linking NMDA receptor activation to neuronal ROS generation by NADPH oxidase (Brennan et al, 2009;Girouard et al, 2009).…”

Section: Discussionsupporting

confidence: 90%

“…Previously, mitochondria were considered the major source of ROS in epilepsy (Waldbaum and Patel, 2010). However, recent data from our group and others have found that seizure activity induces ROS generation independent of mitochondria, through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Kim et al, 2013;Kovac et al, 2014). In keeping with other studies we have shown that the NMDA receptor opening leads to ROS production through NADPH oxidase (Brennan et al, 2009;Kovac et al, 2014).…”

Section: Introductionsupporting

confidence: 65%

“…In keeping with other studies we have shown that the NMDA receptor opening leads to ROS production through NADPH oxidase (Brennan et al, 2009;Kovac et al, 2014). Although the in vitro data are compelling, the in vivo studies showing ROS production via NADPH oxidase used chemoconvulsant epilepsy models (Pestana et al, 2010;Kim et al, 2013). In these models the chemoconvulsant pilocarpine is a significant confounder, as pilocarpine can have a direct impact on ROS generation through the interaction between muscarinic receptors and ROS (Tsutsumi et al, 2008).…”

Section: Introductionmentioning

confidence: 62%

“…Previous studies looking into free radical generation in epilepsy used chemoconvulsants to evoke seizure-like activity, hampering the distinction between seizureinduced and pharmacologically-induced free radical generation (Pestana et al, 2010;Kim et al, 2013). In addition, previous studies relied on indirect information obtained from free radical scavengers such as glutathione levels, or enzymes involved in free radical processing such as superoxide dismutase in brain homogenates (for a more comprehensive review see (Shin et al, 2011)).…”

Section: Discussionmentioning

confidence: 98%

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Status epilepticus results in persistent overproduction of reactive oxygen species, inhibition of which is neuroprotective

et al. 2015

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Section: Discussionsupporting

confidence: 90%

Section: Introductionsupporting

confidence: 65%

Section: Introductionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 98%

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Status epilepticus results in persistent overproduction of reactive oxygen species, inhibition of which is neuroprotective

et al. 2015

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“…Inhibition of NADPH oxidase can neuroprotect in in vivo models of status epilepticus [82][83][84]. As previously described ROS and consequent peroxynitrite formation can contribute to cell death though lipid peroxidation, inactivation of enzymes, mPTP opening and DNA damage.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 67%

Pathophysiology of status epilepticus

Walker¹

2018

Neuroscience Letters

109

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Status epilepticus (SE) is the maximal expression of epilepsy with a high morbidity and mortality. It occurs due to the failure of mechanisms that terminate seizures.Both human and animal data indicate that the longer a seizure lasts, the less likely it is to stop. Recent evidence suggests that there is a critical transition from an ictal to a post-ictal state, associated with a transition from a spatio-temporally desynchronized state to a highly synchronized state, respectively.As SE continues, it becomes progressively resistant to drugs, in particular benzodiazepines due partly to NMDA receptor-dependent internalization of GABA (A) receptors. Moreover, excessive calcium entry into neurons through excessive NMDA receptor activation results in activation of nitric oxide synthase, calpains, and NADPH oxidase. The latter enzyme plays a critical part in the generation of seizuredependent reactive oxygen species. Calcium also accumulates in mitochondria resulting in mitochondrial failure (decreased ATP production), and opening of the mitochondrial permeability transition pore. Together these changes result in status epilepticus-dependent neuronal death via several pathways. Multiple downstream mechanisms including inflammation, break down of the blood-brain barrier, and changes in gene expression can contribute to later pathological processes including chronic epilepsy and cognitive decline.

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Blood–Brain Barrier Mechanisms in Stroke and Trauma

Cao

Takase

et al. 2020

Handbook of Experimental Pharmacology

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Post-treatment of an NADPH oxidase inhibitor prevents seizure-induced neuronal death

Cited by 64 publications

References 41 publications

Status epilepticus results in persistent overproduction of reactive oxygen species, inhibition of which is neuroprotective

Status epilepticus results in persistent overproduction of reactive oxygen species, inhibition of which is neuroprotective

Pathophysiology of status epilepticus

Blood–Brain Barrier Mechanisms in Stroke and Trauma

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