The rearrangement of filamentous actin in mossy fiber synapses in pentylenetetrazol-kindled C57BL/6 mice

Zhang, Yanfeng; Li, Shu-Lei; Xiong, Tianqing; Yang, Liman; Li, Yongnan; Tan, Bai-Hong; Li, Qun; li, Yan-Chao

doi:10.1016/j.eplepsyres.2013.10.019

Cited by 7 publications

(12 citation statements)

References 38 publications

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“…Reorganized F-actin networks have been postulated to lead to the long-term stabilization of synaptic changes and consolidation of enhanced neuronal activity. Thus, alterations in F-actin network may be related to the aberrant hyperexcitability that is observed in epilepsy [19]. Rac1 and RhoA were significantly upregulated in the pentylenetetrazole kindling model and play a role in aberrant mossy fiber sprouting [20].…”

Section: Introductionmentioning

confidence: 99%

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

et al. 2016

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Epileptogenesis is a process triggered by initial environmental or genetic factors that result in epilepsy and may continue during disease progression. Important parts of this process include changes in transcriptome and the pathological rewiring of neuronal circuits that involves changes in neuronal morphology. Mammalian/mechanistic target of rapamycin (mTOR) is upregulated by proconvulsive drugs, e.g., kainic acid, and is needed for progression of epileptogenesis, but molecular aspects of its contribution are not fully understood. Since mTOR can modulate transcription, we tested if rapamycin, an mTOR complex 1 inhibitor, affects kainic acid-evoked transcriptome changes. Using microarray technology, we showed that rapamycin inhibits the kainic acid-induced expression of multiple functionally heterogeneous genes. We further focused on engulfment and cell motility 1 (Elmo1), which is a modulator of actin dynamics and therefore could contribute to pathological rewiring of neuronal circuits during epileptogenesis. We showed that prolonged overexpression of Elmo1 in cultured hippocampal neurons increased axonal growth, decreased dendritic spine density, and affected their shape. In conclusion, data presented herein show that increased mTORC1 activity in response to kainic acid has no global effect on gene expression. Instead, our findings suggest that mTORC1 inhibition may affect development of epilepsy, by modulating expression of specific subset of genes, including Elmo1, and point to a potential role for Elmo1 in morphological changes that accompany epileptogenesis.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-016-9821-6) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

et al. 2016

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“…For staining of PSD95, pretreatment with pepsin was used to improve the detection 25 . Details have been described previously 6 , 23 .…”

Section: Methodsmentioning

confidence: 99%

“…Preparation of samples was performed according to a previously published method [6,23]. One hour after the stop of seizures, the animals were anesthetized and sacrificed, followed by 4% paraformaldehyde perfusion.…”

Section: Sample Preparationsmentioning

confidence: 99%

“…As mentioned previously [6,23], we labeled F-actin specifically with phalloidin conjugated to Alexa 488. After a thirty-minute pretreatment with 0.3% Triton X-100, sections were incubated in Alexa 488-labeled phalloidin (1:100; A12379, Molecular Probes) in the dark overnight at 4℃.…”

Section: F-actin Labelingmentioning

confidence: 99%

“…We measured at least 3 fields for each hippocampal subregion in each animal. The numbers of pyramidal cells in areas CA1 and CA3 were counted as in the previous description [23,24,27]. In brief, neurons in the subregions of CA1 and CA3b were counted in a defined rectangular field using ImageJ software.…”

Section: Image Acquisition and Data Analysismentioning

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

Yang

Xiong

et al. 2019

Epilepsy Research

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The rearrangement of filamentous actin in mossy fiber synapses in pentylenetetrazol-kindled C57BL/6 mice

Cited by 7 publications

References 38 publications

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons

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

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

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