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Molecular and Cellular Mechanisms of Epilepsy

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 31255

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Dr. Aleksey Zaitsev

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Laboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry, 194223 Saint Petersburg, Russia
Interests: electrophysiology; neurophysiology; neurobiology and brain physiology; neurobiology; neuropharmacology; cellular neuroscience physiology; neuron; neuroscience; brain
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Prof. Dr. Roustem Khazipov

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National Institute of Health and Medical Research, Port-Royal Hospital, 123 Bd de Port-Royal, 75014 Paris, France
Interests: neuronal network activity; electrical activity in brain; GABA; neurotransmitter gamma-aminobutyric acid

Special Issue Information

Dear Colleagues,

Despite the availability of many antiepileptic drugs, more than 30% of patients with epilepsy, especially temporal lobe epilepsy, continue to experience seizures. The most rational therapeutic option for drug-resistant epilepsy is the prevention of the development and progression of epilepsy. Prevention has to be grounded in the understanding of the pathophysiological mechanisms leading to epilepsy. In the case of temporal lobe epilepsy, our knowledge of the possible causes is still insufficient. In recent years, many breakthroughs have been made in identifying cellular and molecular alterations linked to severe epilepsy. These alterations include but are not limited to 1) loss of principal cells and interneurons and neurogenesis, including changes in morphology and neuronal firing patterns related with altered composition or expression of receptors and channels; 2) gliosis, including changes in the functioning of glial cells and neuron-astrocyte interactions; 3) loss of the integrity of blood–brain barrier and neuroinflammation. All these histopathological changes are suspected to contribute to epileptogenesis and could be important targets for preventive therapies.

This special issue "Molecular and Cellular Mechanisms of Epilepsy”, will comprise a selection of research papers and reviews covering various aspects of molecular and cellular biology of epilepsy models. Studies on bioactive molecules modulating epileptogenesis will also be considered.

Dr. Aleksey Zaitsev
Prof. Dr. Roustem Khazipov
Guest Editors

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Keywords

epilepsy
epilepsy models
epileptogenesis
preventing epilepsy
neuroinflammation
neuroprotection
synaptic plasticity
neuron–astrocyte interaction

Published Papers (12 papers)

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Editorial

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3 pages, 187 KiB

Open AccessEditorial

Molecular and Cellular Mechanisms of Epilepsy

by Aleksey V. Zaitsev and Roustem Khazipov

Int. J. Mol. Sci. 2023, 24(15), 12415; https://doi.org/10.3390/ijms241512415 - 4 Aug 2023

Viewed by 1071

Abstract

Despite the availability of a large number of antiepileptic drugs, about 30% of patients with epilepsy, especially temporal lobe epilepsy (TLE), continue to experience seizures [...] Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

Research

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19 pages, 8285 KiB

Open AccessArticle

Optogenetic Low-Frequency Stimulation of Principal Neurons, but Not Parvalbumin-Positive Interneurons, Prevents Generation of Ictal Discharges in Rodent Entorhinal Cortex in an In Vitro 4-Aminopyridine Model

by Elena Y. Proskurina, Anton V. Chizhov and Aleksey V. Zaitsev

Int. J. Mol. Sci. 2023, 24(1), 195; https://doi.org/10.3390/ijms24010195 - 22 Dec 2022

Cited by 7 | Viewed by 1687

Abstract

Low-frequency electrical stimulation is used to treat some drug-resistant forms of epilepsy. Despite the effectiveness of the method in suppressing seizures, there is a considerable risk of side effects. An optogenetic approach allows the targeting of specific populations of neurons, which can increase the effectiveness and safety of low-frequency stimulation. In our study, we tested the efficacy of the suppression of ictal activity in entorhinal cortex slices in a 4-aminopyridine model with three variants of low-frequency light stimulation (LFLS): (1) activation of excitatory and inhibitory neurons (on Thy1-ChR2-YFP mice), (2) activation of inhibitory interneurons only (on PV-Cre mice after virus injection with channelrhodopsin2 gene), and (3) hyperpolarization of excitatory neurons (on Wistar rats after virus injection with archaerhodopsin gene). Only in the first variant did simultaneous LFLS of excitatory and inhibitory neurons replace ictal activity with interictal activity. We suggest that LFLS caused changes in the concentration gradients of K⁺ and Na⁺ cations across the neuron membrane, which activated Na-K pumping. According to the mathematical modeling, the increase in Na-K pump activity in neurons induced by LFLS led to an antiepileptic effect. Thus, a less specific and generalized optogenetic effect on entorhinal cortex neurons was more effective in suppressing ictal activity in the 4-aminopyridine model. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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17 pages, 2953 KiB

Open AccessArticle

The Brain Protein Acylation System Responds to Seizures in the Rat Model of PTZ-Induced Epilepsy

by Lev G. Zavileyskiy, Vasily A. Aleshin, Thilo Kaehne, Irina S. Karlina, Artem V. Artiukhov, Maria V. Maslova, Anastasia V. Graf and Victoria I. Bunik

Int. J. Mol. Sci. 2022, 23(20), 12302; https://doi.org/10.3390/ijms232012302 - 14 Oct 2022

Cited by 5 | Viewed by 2074

Abstract

Abnormal energy expenditure during seizures and metabolic regulation through post-translational protein acylation suggest acylation as a therapeutic target in epilepsy. Our goal is to characterize an interplay between the brain acylation system components and their changes after seizures. In a rat model of pentylenetetrazole (PTZ)-induced epilepsy, we quantify 43 acylations in 29 cerebral cortex proteins; levels of NAD⁺; expression of NAD⁺-dependent deacylases (SIRT2, SIRT3, SIRT5); activities of the acyl-CoA-producing/NAD⁺-utilizing complexes of 2-oxoacid dehydrogenases. Compared to the control group, acylations of 14 sites in 11 proteins are found to differ significantly after seizures, with six of the proteins involved in glycolysis and energy metabolism. Comparing the single and chronic seizures does not reveal significant differences in the acylations, pyruvate dehydrogenase activity, SIRT2 expression or NAD⁺. On the contrary, expression of SIRT3, SIRT5 and activity of 2-oxoglutarate dehydrogenase (OGDH) decrease in chronic seizures vs. a single seizure. Negative correlations between the protein succinylation/glutarylation and SIRT5 expression, and positive correlations between the protein acetylation and SIRT2 expression are shown. Our findings unravel involvement of SIRT5 and OGDH in metabolic adaptation to seizures through protein acylation, consistent with the known neuroprotective role of SIRT5 and contribution of OGDH to the Glu/GABA balance perturbed in epilepsy. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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16 pages, 1811 KiB

Open AccessArticle

Elevated Serum Cortisol Levels in Patients with Focal Epilepsy, Depression, and Comorbid Epilepsy and Depression

by Tatyana A. Druzhkova, Alexander A. Yakovlev, Flora K. Rider, Mikhail S. Zinchuk, Alla B. Guekht and Natalia V. Gulyaeva

Int. J. Mol. Sci. 2022, 23(18), 10414; https://doi.org/10.3390/ijms231810414 - 8 Sep 2022

Cited by 7 | Viewed by 2887

Abstract

Background: The hypothalamic-pituitary-adrenal (HPA) axis, inflammatory processes and neurotrophic factor systems are involved in pathogenesis of both epilepsy and depressive disorders. The study aimed to explore these systems in patients with focal epilepsy (PWE, n = 76), epilepsy and comorbid depression (PWCED n = 48), and major depressive disorder (PWMDD, n = 62) compared with healthy controls (HC, n = 78). Methods: Parameters of the HPA axis, neurotrophic factors, and TNF-α were measured in blood serum along with the hemogram. Results: Serum cortisol level was augmented in PWE, PWCED, and PWMDD compared with HC and was higher in PWMDD than in PWE. Serum cortisol negatively correlated with Mini–Mental State Examination (MMSE) score in PWE, and positively with depression inventory–II (BDI-II) score in PWMDD. Only PWMDD demonstrated elevated plasma ACTH. Serum TNF-α, lymphocytes, and eosinophils were augmented in PWMDD; monocytes elevated in PWE and PWCED, while neutrophils were reduced in PWE and PWMDD. Serum BDNF was decreased in PWE and PWCED, CNTF was elevated in all groups of patients. In PWE, none of above indices depended on epilepsy etiology. Conclusions: The results confirm the involvement of HPA axis and inflammatory processes in pathogenesis of epilepsy and depression and provide new insights in mechanisms of epilepsy and depression comorbidity. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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21 pages, 8297 KiB

Open AccessArticle

Glucocorticoid Receptor β Isoform Predominates in the Human Dysplastic Brain Region and Is Modulated by Age, Sex, and Antiseizure Medication

by Rosemary Westcott, Natalie Chung, Arnab Ghosh, Lisa Ferguson, William Bingaman, Imad M. Najm and Chaitali Ghosh

Int. J. Mol. Sci. 2022, 23(9), 4940; https://doi.org/10.3390/ijms23094940 - 29 Apr 2022

Cited by 5 | Viewed by 1914

Abstract

The glucocorticoid receptor (GR) at the blood–brain barrier (BBB) is involved in the pathogenesis of drug-resistant epilepsy with focal cortical dysplasia (FCD); however, the roles of GR isoforms GRα and GRβ in the dysplastic brain have not been revealed. We utilized dysplastic/epileptic and non-dysplastic brain tissue from patients who underwent resective epilepsy surgery to identify the GRα and GRβ levels, subcellular localization, and cellular specificity. BBB endothelial cells isolated from the dysplastic brain tissue (EPI-ECs) were used to decipher the key BBB proteins related to drug regulation and BBB integrity compared to control and transfected GRβ-overexpressed BBB endothelial cells. GRβ was upregulated in dysplastic compared to non-dysplastic tissues, and an imbalance of the GRα/GRβ ratio was significant in females vs. males and in patients > 45 years old. In EPI-ECs, the subcellular localization and expression patterns of GRβ, Hsp90, CYP3A4, and CYP2C9 were consistent with GRβ+ brain endothelial cells. Active matrix metalloproteinase levels and activity increased, whereas claudin-5 levels decreased in both EPI-ECs and GRβ+ endothelial cells. In conclusion, the GRβ has a major effect on dysplastic BBB functional proteins and is age and gender-dependent, suggesting a critical role of brain GRβ in dysplasia as a potential biomarker and therapeutic target in epilepsy. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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16 pages, 1693 KiB

Open AccessArticle

The Anti-Epileptic Effects of Carbenoxolone In Vitro and In Vivo

by Anna Volnova, Vassiliy Tsytsarev, Olga Ganina, Grace E. Vélez-Crespo, Janaina M. Alves, Alla Ignashchenkova and Mikhail Inyushin

Int. J. Mol. Sci. 2022, 23(2), 663; https://doi.org/10.3390/ijms23020663 - 8 Jan 2022

Cited by 18 | Viewed by 2423

Abstract

Gap junctions (GJs) are intercellular junctions that allow the direct transfer of ions and small molecules between neighboring cells, and GJs between astrocytes play an important role in the development of various pathologies of the brain, including regulation of the pathological neuronal synchronization underlying epileptic seizures. Recently, we found that a pathological change is observed in astrocytes during the ictal and interictal phases of 4-aminopyridin (4-AP)-elicited epileptic activity in vitro, which was correlated with neuronal synchronization and extracellular epileptic electrical activity. This finding raises the question: Does this signal depend on GJs between astrocytes? In this study we investigated the effect of the GJ blocker, carbenoxolone (CBX), on epileptic activity in vitro and in vivo. Based on the results obtained, we came to the conclusion that the astrocytic syncytium formed by GJ-associated astrocytes, which is responsible for the regulation of potassium, affects the formation of epileptic activity in astrocytes in vitro and epileptic seizure onset. This effect is probably an important, but not the only, mechanism by which CBX suppresses epileptic activity. It is likely that the mechanisms of selective inhibition of GJs between astrocytes will show important translational benefits in anti-epileptic therapies. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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21 pages, 10211 KiB

Open AccessArticle

Impairments of Long-Term Synaptic Plasticity in the Hippocampus of Young Rats during the Latent Phase of the Lithium-Pilocarpine Model of Temporal Lobe Epilepsy

by Tatyana Y. Postnikova, Georgy P. Diespirov, Dmitry V. Amakhin, Elizaveta N. Vylekzhanina, Elena B. Soboleva and Aleksey V. Zaitsev

Int. J. Mol. Sci. 2021, 22(24), 13355; https://doi.org/10.3390/ijms222413355 - 12 Dec 2021

Cited by 18 | Viewed by 3145

Abstract

Status epilepticus (SE) causes persistent abnormalities in the functioning of neuronal networks, often resulting in worsening epileptic seizures. Many details of cellular and molecular mechanisms of seizure-induced changes are still unknown. The lithium–pilocarpine model of epilepsy in rats reproduces many features of human temporal lobe epilepsy. In this work, using the lithium–pilocarpine model in three-week-old rats, we examined the morphological and electrophysiological changes in the hippocampus within a week following pilocarpine-induced seizures. We found that almost a third of the neurons in the hippocampus and dentate gyrus died on the first day, but this was not accompanied by impaired synaptic plasticity at that time. A diminished long-term potentiation (LTP) was observed following three days, and the negative effect of SE on plasticity increased one week later, being accompanied by astrogliosis. The attenuation of LTP was caused by the weakening of N-methyl-D-aspartate receptor (NMDAR)-dependent signaling. NMDAR-current was more than two-fold weaker during high-frequency stimulation in the post-SE rats than in the control group. Application of glial transmitter D-serine, a coagonist of NMDARs, allows the enhancement of the NMDAR-dependent current and the restoration of LTP. These results suggest that the disorder of neuron–astrocyte interactions plays a critical role in the impairment of synaptic plasticity. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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24 pages, 8916 KiB

Open AccessArticle

Human Stem Cell-Derived GABAergic Interneurons Establish Efferent Synapses onto Host Neurons in Rat Epileptic Hippocampus and Inhibit Spontaneous Recurrent Seizures

by Eliška Waloschková, Ana Gonzalez-Ramos, Apostolos Mikroulis, Jan Kudláček, My Andersson, Marco Ledri and Merab Kokaia

Int. J. Mol. Sci. 2021, 22(24), 13243; https://doi.org/10.3390/ijms222413243 - 8 Dec 2021

Cited by 11 | Viewed by 3340

Abstract

Epilepsy is a complex disorder affecting the central nervous system and is characterised by spontaneously recurring seizures (SRSs). Epileptic patients undergo symptomatic pharmacological treatments, however, in 30% of cases, they are ineffective, mostly in patients with temporal lobe epilepsy. Therefore, there is a need for developing novel treatment strategies. Transplantation of cells releasing γ-aminobutyric acid (GABA) could be used to counteract the imbalance between excitation and inhibition within epileptic neuronal networks. We generated GABAergic interneuron precursors from human embryonic stem cells (hESCs) and grafted them in the hippocampi of rats developing chronic SRSs after kainic acid-induced status epilepticus. Using whole-cell patch-clamp recordings, we characterised the maturation of the grafted cells into functional GABAergic interneurons in the host brain, and we confirmed the presence of functional inhibitory synaptic connections from grafted cells onto the host neurons. Moreover, optogenetic stimulation of grafted hESC-derived interneurons reduced the rate of epileptiform discharges in vitro. We also observed decreased SRS frequency and total time spent in SRSs in these animals in vivo as compared to non-grafted controls. These data represent a proof-of-concept that hESC-derived GABAergic neurons can exert a therapeutic effect on epileptic animals presumably through establishing inhibitory synapses with host neurons. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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Review

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18 pages, 1923 KiB

Open AccessReview

Developing Novel Experimental Models of m-TORopathic Epilepsy and Related Neuropathologies: Translational Insights from Zebrafish

by Murilo S. de Abreu, Konstantin A. Demin, Maria M. Kotova, Foad Mirzaei, Sanobar Shariff, Burhan Kantawala, Ksenia V. Zakharchenko, Tatiana O. Kolesnikova, Karen Dilbaryan, Artem Grigoryan, Konstantin B. Yenkoyan and Allan V. Kalueff

Int. J. Mol. Sci. 2023, 24(2), 1530; https://doi.org/10.3390/ijms24021530 - 12 Jan 2023

Cited by 5 | Viewed by 2349

Abstract

The mammalian target of rapamycin (mTOR) is an important molecular regulator of cell growth and proliferation. Brain mTOR activity plays a crucial role in synaptic plasticity, cell development, migration and proliferation, as well as memory storage, protein synthesis, autophagy, ion channel expression and axonal regeneration. Aberrant mTOR signaling causes a diverse group of neurological disorders, termed ‘mTORopathies’. Typically arising from mutations within the mTOR signaling pathway, these disorders are characterized by cortical malformations and other neuromorphological abnormalities that usually co-occur with severe, often treatment-resistant, epilepsy. Here, we discuss recent advances and current challenges in developing experimental models of mTOR-dependent epilepsy and other related mTORopathies, including using zebrafish models for studying these disorders, as well as outline future directions of research in this field. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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18 pages, 415 KiB

Open AccessReview

Towards Zebrafish Models of CNS Channelopathies

by Tatiana O. Kolesnikova, Konstantin A. Demin, Fabiano V. Costa, Konstantin N. Zabegalov, Murilo S. de Abreu, Elena V. Gerasimova and Allan V. Kalueff

Int. J. Mol. Sci. 2022, 23(22), 13979; https://doi.org/10.3390/ijms232213979 - 12 Nov 2022

Cited by 4 | Viewed by 1906

Abstract

Channelopathies are a large group of systemic disorders whose pathogenesis is associated with dysfunctional ion channels. Aberrant transmembrane transport of K⁺, Na⁺, Ca²⁺ and Cl⁻ by these channels in the brain induces central nervous system (CNS) channelopathies, most commonly including epilepsy, but also migraine, as well as various movement and psychiatric disorders. Animal models are a useful tool for studying pathogenesis of a wide range of brain disorders, including channelopathies. Complementing multiple well-established rodent models, the zebrafish (Danio rerio) has become a popular translational model organism for neurobiology, psychopharmacology and toxicology research, and for probing mechanisms underlying CNS pathogenesis. Here, we discuss current prospects and challenges of developing genetic, pharmacological and other experimental models of major CNS channelopathies based on zebrafish. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

20 pages, 2193 KiB

Open AccessReview

Mechanisms Involved in Epileptogenesis in Alzheimer’s Disease and Their Therapeutic Implications

by Miren Altuna, Gonzalo Olmedo-Saura, María Carmona-Iragui and Juan Fortea

Int. J. Mol. Sci. 2022, 23(8), 4307; https://doi.org/10.3390/ijms23084307 - 13 Apr 2022

Cited by 17 | Viewed by 3466

Abstract

Epilepsy and Alzheimer’s disease (AD) incidence increases with age. There are reciprocal relationships between epilepsy and AD. Epilepsy is a risk factor for AD and, in turn, AD is an independent risk factor for developing epilepsy in old age, and abnormal AD biomarkers in PET and/or CSF are frequently found in late-onset epilepsies of unknown etiology. Accordingly, epilepsy and AD share pathophysiological processes, including neuronal hyperexcitability and an early excitatory–inhibitory dysregulation, leading to dysfunction in the inhibitory GABAergic and excitatory glutamatergic systems. Moreover, both β-amyloid and tau protein aggregates, the anatomopathological hallmarks of AD, have proepileptic effects. Finally, these aggregates have been found in the resection material of refractory temporal lobe epilepsies, suggesting that epilepsy leads to amyloid and tau aggregates. Some epileptic syndromes, such as medial temporal lobe epilepsy, share structural and functional neuroimaging findings with AD, leading to overlapping symptomatology, such as episodic memory deficits and toxic synergistic effects. In this respect, the existence of epileptiform activity and electroclinical seizures in AD appears to accelerate the progression of cognitive decline, and the presence of cognitive decline is much more prevalent in epileptic patients than in elderly patients without epilepsy. Notwithstanding their clinical significance, the diagnosis of clinical seizures in AD is a challenge. Most are focal and manifest with an altered level of consciousness without motor symptoms, and are often interpreted as cognitive fluctuations. Finally, despite the frequent association of epilepsy and AD dementia, there is a lack of clinical trials to guide the use of antiseizure medications (ASMs). There is also a potential role for ASMs to be used as disease-modifying drugs in AD. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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21 pages, 678 KiB

Open AccessReview

Non-Coding RNAs: New Biomarkers and Therapeutic Targets for Temporal Lobe Epilepsy

by Ida Manna, Francesco Fortunato, Selene De Benedittis, Ilaria Sammarra, Gloria Bertoli, Angelo Labate and Antonio Gambardella

Int. J. Mol. Sci. 2022, 23(6), 3063; https://doi.org/10.3390/ijms23063063 - 11 Mar 2022

Cited by 9 | Viewed by 3126

Abstract

Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy; it is considered a network disorder associated with structural changes. Incomplete knowledge of the pathological changes in TLE complicates a therapeutic approach; indeed, 30 to 50% of patients with TLE are refractory to drug treatment. Non-coding RNAs (ncRNAs), acting as epigenetic factors, participate in the regulation of the pathophysiological processes of epilepsy and are dysregulated during epileptogenesis. Abnormal expression of ncRNA is observed in patients with epilepsy and in animal models of epilepsy. Furthermore, ncRNAs could also be used as biomarkers for the diagnosis and prognosis of treatment response in epilepsy. In summary, ncRNAs can represent important mechanisms and targets for the modulation of brain excitability and can provide information on pathomechanisms, biomarkers and novel therapies for epilepsy. In this review, we summarize the latest research advances concerning mainly molecular mechanisms, regulated by ncRNA, such as synaptic plasticity, inflammation and apoptosis, already associated with the pathogenesis of TLE. Moreover, we discuss the role of ncRNAs, such as microRNAs, long non-coding RNAs and circular RNAs, in the pathophysiology of epilepsy, highlighting their use as potential biomarkers for future therapeutic approaches. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy)

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