Detection of c-Fos Expression in the Brains of Animals with a Pilocarpine Model of Temporal Lobe Epilepsy

Sinel’nikova, V. V.; Shubina, Liubov; Goltyaev, M. V.; Loseva, E. V.; Kichigina, V. F.

doi:10.1007/s11055-013-9853-6

Cited by 6 publications

(8 citation statements)

References 27 publications

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“…c‐Fos, an immediate early gene, was associated with the changes of neuronal activities, including structure, and function of neurons in the nervous system of mammalian (Watanabe et al, ). During the development of the status epilepticus, c‐Fos expression was high in neuronal populations (Sinel'nikova, Shubina, Gol'tiaev, Loseva, & Kichigina, ). In addition, Gorter et al () indicated that abnormality of MAPK signaling was closely related to a variety of cancers and various neurodegenerative diseases, including Alzheimer's, Parkinson's, and some motor neuron diseases.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Effects of microRNA‐129 and its target gene c‐Fos on proliferation and apoptosis of hippocampal neurons in rats with epilepsy via the MAPK signaling pathway

Zhang

Lü

et al. 2018

Journal Cellular Physiology

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This study aims to investigate the effect of microRNA-129 (miR-129) on proliferation and apoptosis of hippocampal neurons in epilepsy rats by targeting c-Fos via the MAPK signaling pathway. Thirty rats were equally classified into a model group (successfully established as chronic epilepsy models) and a normal group. Expression of miR-129, c-Fos, bax, and MAPK was detected by RT-qPCR and Western blotting. Hippocampal neurons were assigned into normal, blank, negative control (NC), miR-129 mimic, miR-129 inhibitor, siRNA-c-Fos, miR-129 inhibitor+siRNA-c-Fos groups. The targeting relationship between miR-129 and c-Fos was predicted and verified by bioinformatics websites and dual-luciferase reporter gene assay. Cell proliferation after transfection was measured by MTT assay, and cell cycle and apoptosis by flow cytometry. c-Fos is a potential target gene of miR-129. Compared with the normal group, the other six groups showed a decreased miR-129 expression; increased expression of expression of c-Fos, Bax, and MAPK; decreased proliferation; accelerated apoptosis; more cells arrested in the G1 phase; and fewer cells arrested in the S phase. Compared with the blank and NC groups, the miR-129 mimic group and the siRNA-c-Fos group showed decreased expression of c-Fos, Bax, and MAPK, increased cells proliferation, and decreased cell apoptosis, fewer cells arrested in the G1 phase and more cells arrested in the S phase. However, the miR-129 inhibitor groups showed reverse consequences. This study suggests that miR-129 could inhibit the occurrence and development of epilepsy by repressing c-Fos expression through inhibiting the MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Retracted: Effects of microRNA‐129 and its target gene c‐Fos on proliferation and apoptosis of hippocampal neurons in rats with epilepsy via the MAPK signaling pathway

Zhang

Lü

et al. 2018

Journal Cellular Physiology

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“…Although many brain regions are affected, serial MRI shows the earliest changes in the piriform and entorhinal cortex, as early as 6 h after the status epilepticus ( 163 , 164 ), reflecting cellular edema, and neuronal loss in these regions ( 165 ). Cellular hyperactivity, imaged by c-fos expression, is first seen (at 30 min) at the piriform cortex, olfactory tubercle, thalamus, caudate, and lateral habenula, with later changes (at 60–90 min) in hippocampus, amygdala, and basal ganglia ( 166 ). Early neuronal loss and gliosis occur in the piriform cortex, hippocampus, amydala, thalamus, and substantia nigra ( 167 ).…”

Section: Piriform Cortex Is Susceptible To Seizure-induced Injury Andmentioning

confidence: 99%

The Piriform Cortex and Human Focal Epilepsy

2014

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It is surprising that the piriform cortex, when compared to the hippocampus, has been given relatively little significance in human epilepsy. Like the hippocampus, it has a phylogenetically preserved three-layered cortex that is vulnerable to excitotoxic injury, has broad connections to both limbic and cortical areas, and is highly epileptogenic – being critical to the kindling process. The well-known phenomenon of early olfactory auras in temporal lobe epilepsy highlights its clinical relevance in human beings. Perhaps because it is anatomically indistinct and difficult to approach surgically, as it clasps the middle cerebral artery, it has, until now, been understandably neglected. In this review, we emphasize how its unique anatomical and functional properties, as primary olfactory cortex, predispose it to involvement in focal epilepsy. From recent convergent findings in human neuroimaging, clinical epileptology, and experimental animal models, we make the case that the piriform cortex is likely to play a facilitating and amplifying role in human focal epileptogenesis, and may influence progression to epileptic intractability.

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“…While SE and ECS seizures clearly manifest differently in EEG and behavioral measures, both types of seizures have been shown to recruit the hippocampal formation (Ingvar, 1986; Morinobu et al, 1997; Hsieh et al, 1998; Ji et al, 1998; Scorza et al, 2002; Dyrvig et al, 2012; Sinel’nikova et al, 2013). Since persons with epilepsy normally present with acute seizures as opposed to SE, our acute ECS studies may model human seizures with higher validity than SE or chronic stimulation protocols (by design, these tend to model epileptogenesis rather than acute seizures).…”

Section: Discussionmentioning

confidence: 99%

Electroconvulsive Shock Enhances Responsive Motility and Purinergic Currents in Microglia in the Mouse Hippocampus

Sepulveda-Rodriguez

Khan

et al. 2019

eNeuro

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Microglia are in a privileged position to both affect and be affected by neuroinflammation, neuronal activity and injury, which are all hallmarks of seizures and the epilepsies. Hippocampal microglia become activated after prolonged, damaging seizures known as status epilepticus (SE). However, since SE causes both hyperactivity and injury of neurons, the mechanisms triggering this activation remain unclear, as does the relevance of the microglial activation to the ensuing epileptogenic processes. In this study, we use electroconvulsive shock (ECS) to study the effect of neuronal hyperactivity without neuronal degeneration on mouse hippocampal microglia. Unlike SE, ECS did not alter hippocampal CA1 microglial density, morphology, or baseline motility. In contrast, both ECS and SE produced a similar increase in ATP-directed microglial process motility in acute slices, and similarly upregulated expression of the chemokine CC motif chemokine ligand 2 (CCL2). Whole-cell patch-clamp recordings of hippocampal CA1sr microglia showed that ECS enhanced purinergic currents mediated by P2X7 receptors in the absence of changes in passive properties or voltage-gated currents, or changes in receptor expression. This differs from previously described alterations in intrinsic characteristics which coincided with enhanced purinergic currents following SE. These ECS-induced effects point to a "seizure signature" in hippocampal microglia characterized by altered purinergic signaling. These data demonstrate that ictal activity per se can drive alterations in microglial physiology without neuronal injury. These physiological changes, which up until now have been associated with prolonged and damaging seizures, are of added interest as they may be relevant to electroconvulsive therapy (ECT), which remains a gold-standard treatment for depression.

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Detection of c-Fos Expression in the Brains of Animals with a Pilocarpine Model of Temporal Lobe Epilepsy

Cited by 6 publications

References 27 publications

Retracted: Effects of microRNA‐129 and its target gene c‐Fos on proliferation and apoptosis of hippocampal neurons in rats with epilepsy via the MAPK signaling pathway

Retracted: Effects of microRNA‐129 and its target gene c‐Fos on proliferation and apoptosis of hippocampal neurons in rats with epilepsy via the MAPK signaling pathway

The Piriform Cortex and Human Focal Epilepsy

Electroconvulsive Shock Enhances Responsive Motility and Purinergic Currents in Microglia in the Mouse Hippocampus

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