Dexamethasone ameliorates the damage of hippocampal filamentous actin cytoskeleton but is not sufficient to cease epileptogenesis in pilocarpine induced epileptic mice

Yang, Ning; Li, Yanchao; Xiong, Tianqing; Chen, Ling-Meng; Yu, Zhengquan; Liang, Jing; Hao, Yunpeng; Ma, Dihui; Zhang, Yanfeng

doi:10.1016/j.eplepsyres.2019.04.009

Cited by 7 publications

(13 citation statements)

References 49 publications

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“…In a penicillin-induced model, DEX at dosages of 1, 3, and 10 mg/kg were assessed on epileptiform activity, and spike frequencies were significantly suppressed by DEX administration at both 3 mg/kg and 10 mg/kg [30]. Consistently, our previous study also showed a protective effect on the epileptic brain with 3 doses of 10 mg/kg DEX during quiescence in the pilocarpine-induced epileptic model [20]. In this study, we performed administration of DEX at a different time point to test the effect of DEX during SE and further studied the effects of glucocorticoids on brain remodeling.…”

Section: Discussionsupporting

confidence: 81%

“…After pilocarpine injection, the behavioral changes of animals in this research were similar to those of previous studies [6,7,20]. As a result, in the PILO and PILO+DEX groups, the ratios of animals that met the SE and survived were 47.62% and 45.83%, and the mortality rates were 42.86% and 25%, respectively.…”

Section: Influence Of Dexamethasone Treatment On Acute Seizures Inducsupporting

confidence: 86%

“…Many reports have stated that glucocorticoids have a protective effect on neuronal loss in epilepsy models [20,42]. Therefore, we explored the changes in hippocampal neurons among groups.…”

Section: Discussionmentioning

confidence: 99%

“…Coincidentally, GRs regulate the morphology and stability of dendritic spines by controlling the dynamic balance of the actin cytoskeleton between depolymerization and polymerization [18]. Our previous study showed that administration of dexamethasone during the latent period reduces damage to the hippocampal filamentous actin cytoskeleton and pyramidal neurons and helps to maintain the synaptic structures but is not sufficient to stop epileptogenesis in a pilocarpine-induced epileptic model [20]. However, it is still unclear how glucocorticoids affect the process of epileptogenesis by regulating the dynamics of the actin cytoskeleton during SE.…”

Section: Ivyspringmentioning

confidence: 99%

“…As described in previous studies, hippocampal pyramidal cells were detected by Anti-NeuN antibody [20,24]. After pretreatment of 10% normal donkey serum with 0.3% Triton X-100 for 30 minutes at room temperature, slices were incubated with rabbit monoclonal anti-NeuN antibody (1:100, ab177487, Abcam, USA) overnight at 4 °C.…”

Section: Hippocampal Pyramidal Cell Quantificationmentioning

confidence: 99%

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Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

et al. 2020

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The filamentous actin (F-actin) cytoskeleton is progressively damaged after status epilepticus (SE), which is related to delayed neuronal death, aberrant recurrent circuits and epileptogenesis. Glucocorticoids regulate dendritic spine remodeling by acting on glucocorticoid receptors and the dynamics of the F-actin cytoskeleton. Our previous study showed that administration of dexamethasone (DEX) in the latent period of the pilocarpine epileptic model reduces damage to the hippocampal filamentous actin cytoskeleton and the loss of hippocampal neurons and aids in maintaining the synaptic structures, but it is not sufficient to stop epileptogenesis. In this work, we focused on the role of glucocorticoids in regulating the hippocampal F-actin cytoskeleton during SE. We examined the abundance of synaptic F-actin, analyzed the hippocampal F-actin/G-actin (F/G) ratio and pCofilin, and evaluated the number of hippocampal neurons and pre/postsynaptic markers in pilocarpine-induced status epilepticus mice with or without administration of dexamethasone (DEX). We found that the latency of Stage 3 seizures increased, the mortality decreased, the damage to the synaptic F-actin cytoskeleton in the hippocampal subfields was significantly attenuated, and a greater number of postsynaptic structures were retained in the hippocampal subfields after treatment with DEX. These results indicate that treatment with dexamethasone stabilizes the synaptic F-actin cytoskeleton and reduces the damage to the brain due to SE. This approach is expected to be beneficial in alleviating delayed neuron damage and the process of epileptogenesis.

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Section: Discussionsupporting

confidence: 81%

Section: Influence Of Dexamethasone Treatment On Acute Seizures Inducsupporting

confidence: 86%

“…Many reports have stated that glucocorticoids have a protective effect on neuronal loss in epilepsy models [20,42]. Therefore, we explored the changes in hippocampal neurons among groups.…”

Section: Discussionmentioning

confidence: 99%

Section: Ivyspringmentioning

confidence: 99%

Section: Hippocampal Pyramidal Cell Quantificationmentioning

confidence: 99%

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Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

et al. 2020

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Microtubule Dynamics and Neuronal Excitability: Advances on Cytoskeletal Components Implicated in Epileptic Phenomena

et al. 2020

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Extensive researches have deepened knowledge on the role of synaptic components in epileptogenesis, but limited attention has been devoted to the potential implication of the cytoskeleton. The study of the development of epilepsy and hyperexcitability states involves molecular, synaptic, and structural alterations of neuronal bioelectric activity. In this paper we aim to explore the neurobiological targets involved in microtubule functioning and cytoskeletal transport, i.e. how dynamic scaffolding of microtubules can influence neuronal morphology and excitability, in order to suggest a potential role for microtubule dynamics in the processes turning a normal neuronal network in a hyperexcited one. Pathophysiological alterations of microtubule dynamics inducing neurodegeneration, network remodeling and relative impairment on synaptic transmission were overviewed. Recent researches were reported on the phosphorylation state of microtubule-associated proteins such as tau in neurodegenerative diseases and epileptic states, but also on the effect of microtubule-active agents influencing cytoskeleton destabilization in epilepsy models. The manipulation of microtubule polymerization was found effective in the modulation of hyperexcitability. In addition, it was considered the importance of microtubules and related neurotrophic factors during neural development since they are essential for the formation of a properly functional neuronal network. Otherwise, this can lead to cognitive deficits, hyperexcitability phenomena and neurodevelopmental disorders. Lastly, we evaluated the role of microtubule dynamics on neuronal efficiency considering their importance in the transport of mitochondria, cellular elements fulfilling energy requirements for neuronal activity, and a putative influence on cannabinoid-mediated neuroprotection. This review provides novel perspectives for the implication of microtubule dynamics in the development of epileptic phenomena.

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Differential DNA Methylation Profiles in Patients with Temporal Lobe Epilepsy and Hippocampal Sclerosis ILAE Type I

et al. 2021

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Dexamethasone ameliorates the damage of hippocampal filamentous actin cytoskeleton but is not sufficient to cease epileptogenesis in pilocarpine induced epileptic mice

Cited by 7 publications

References 49 publications

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

Microtubule Dynamics and Neuronal Excitability: Advances on Cytoskeletal Components Implicated in Epileptic Phenomena

Differential DNA Methylation Profiles in Patients with Temporal Lobe Epilepsy and Hippocampal Sclerosis ILAE Type I

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