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Molecular Research in Epilepsy and Epileptogenesis
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Molecular Research in Epilepsy and Epileptogenesis

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2825

Special Issue Editor

Prof. Dr. Stanisław Jerzy Czuczwar

E-Mail Website
Guest Editor
Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: Alzheimer; epilepsy; stroke

Special Issue Information

Dear Colleauges,

Epilepsy is a neurological disorder affecting approximately 65 million people worldwide. In about 30% of patients with epilepsy, seizures are poorly controlled with antiseizure (antiepileptic) drugs, and drug-resistant epilepsy poses a significant therapeutic problem. Thus, there is a need for more efficient treatments of epilepsy in order to obtain freedom from seizures in a more significant proportion of patients. The molecular targets for available antiseizure drugs have been recognized, and the identification of novel targets and their ligands should result in the development of innovative drugs sharing additional mechanisms of action.

Antiseizure drugs are generally not effective against epileptogenesis that is triggered by an initial insult  (e.g., status epilepticus, head trauma or stroke). The durable process of epileptogenesis has been proven to convert a normally functioning mammalian brain into one generating seizure activity. A possibility arises that stopping or slowing down the progress of epileptogenesis may prevent the occurrence of epilepsy. Certainly, anti-epileptogenic drugs would be most effective prior to seizure activity, so markers for epileptogenesis are required.

Considering what was stated above, this Special Issue on "Molecular Research in Epilepsy and Epileptogenesis" is open to research dealing with molecular mechanisms of seizure activity or epileptogenesis and focused on possible targets for antiseizure and anti-epileptogenic drugs. Original and review papers based on in vitro experiments, animal models of seizures also aimed at the process of epileptogenesis, and clinical studies are invited.

Prof. Dr. Stanisław Jerzy Czuczwar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • epilepsy
  • antiseizure
  • anti-epileptogenic drugs
  • biomarkers

Published Papers (2 papers)

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Research

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18 pages, 2716 KiB  
Article
Age-Dependent Activation of Pannexin1 Function Contributes to the Development of Epileptogenesis in Autosomal Dominant Sleep-related Hypermotor Epilepsy Model Rats
by Kouji Fukuyama, Eishi Motomura and Motohiro Okada
Int. J. Mol. Sci. 2024, 25(3), 1619; https://doi.org/10.3390/ijms25031619 - 28 Jan 2024
Viewed by 627
Abstract
To explore the processes of epileptogenesis/ictogenesis, this study determined the age-dependent development of the functional abnormalities in astroglial transmission associated with pannexin1-hemichannel using a genetic rat model of autosomal dominant sleep-related hypermotor epilepsy (ADSHE) named ‘S286L-TG’. Pannexin1 expression in the plasma membrane of [...] Read more.
To explore the processes of epileptogenesis/ictogenesis, this study determined the age-dependent development of the functional abnormalities in astroglial transmission associated with pannexin1-hemichannel using a genetic rat model of autosomal dominant sleep-related hypermotor epilepsy (ADSHE) named ‘S286L-TG’. Pannexin1 expression in the plasma membrane of primary cultured cortical astrocytes and the orbitofrontal cortex (OFC), which is an ADSHE focus region, were determined using capillary immunoblotting. Astroglial D-serine releases induced by artificial high-frequency oscillation (HFO)-evoked stimulation, the removal of extracellular Ca2+, and the P2X7 receptor agonist (BzATP) were determined using ultra-high performance liquid chromatography (UHPLC). The expressions of pannexin1 in the plasma membrane fraction of the OFC in S286L-TG at four weeks old were almost equivalent when compared to the wild type. The pannexin1 expression in the OFC of the wild type non-statistically decreased age-dependently, whereas that in S286L-TG significantly increased age-dependently, resulting in relatively increasing pannexin1 expression from the 7- (at the onset of interictal discharge) and 10-week-old (after the ADSHE seizure onset) S286L-TG compared to the wild type. However, no functional abnormalities of astroglial pannexin1 expression or D-serine release through the pannexin1-hemichannels from the cultured astrocytes of S286L-TG could be detected. Acutely HFO-evoked stimulation, such as physiological ripple burst (200 Hz) and epileptogenic fast ripple burst (500 Hz), frequency-dependently increased both pannexin1 expression in the astroglial plasma membrane and astroglial D-serine release. Neither the selective inhibitors of pannexin1-hemichannel (10PANX) nor connexin43-hemichannel (Gap19) affected astroglial D-serine release during the resting stage, whereas HFO-evoked D-serine release was suppressed by both inhibitors. The inhibitory effect of 10PANX on the ripple burst-evoked D-serine release was more predominant than that of Gap19, whereas fast ripple burst-evoked D-serine release was predominantly suppressed by Gap19 rather than 10PANX. Astroglial D-serine release induced by acute exposure to BzATP was suppressed by 10PANX but not by Gap19. These results suggest that physiological ripple burst during the sleep spindle plays important roles in the organization of some components of cognition in healthy individuals, but conversely, it contributes to the initial development of epileptogenesis/ictogenesis in individuals who have ADSHE vulnerability via activation of the astroglial excitatory transmission associated with pannexin1-hemichannels. Full article
(This article belongs to the Special Issue Molecular Research in Epilepsy and Epileptogenesis)
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Review

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20 pages, 334 KiB  
Review
Genetic Background of Epilepsy and Antiepileptic Treatments
by Kinga Borowicz-Reutt, Julia Czernia and Marlena Krawczyk
Int. J. Mol. Sci. 2023, 24(22), 16280; https://doi.org/10.3390/ijms242216280 - 14 Nov 2023
Viewed by 1554
Abstract
Advanced identification of the gene mutations causing epilepsy syndromes is expected to translate into faster diagnosis and more effective treatment of these conditions. Over the last 5 years, approximately 40 clinical trials on the treatment of genetic epilepsies have been conducted. As a [...] Read more.
Advanced identification of the gene mutations causing epilepsy syndromes is expected to translate into faster diagnosis and more effective treatment of these conditions. Over the last 5 years, approximately 40 clinical trials on the treatment of genetic epilepsies have been conducted. As a result, some medications that are not regular antiseizure drugs (e.g., soticlestat, fenfluramine, or ganaxolone) have been introduced to the treatment of drug-resistant seizures in Dravet, Lennox-Gastaut, maternally inherited chromosome 15q11.2-q13.1 duplication (Dup 15q) syndromes, and protocadherin 19 (PCDH 19)-clusterig epilepsy. And although the effects of soticlestat, fenfluramine, and ganaxolone are described as promising, they do not significantly affect the course of the mentioned epilepsy syndromes. Importantly, each of these syndromes is related to mutations in several genes. On the other hand, several mutations can occur within one gene, and different gene variants may be manifested in different disease phenotypes. This complex pattern of inheritance contributes to rather poor genotype–phenotype correlations. Hence, the detection of a specific mutation is not synonymous with a precise diagnosis of a specific syndrome. Bearing in mind that seizures develop as a consequence of the predominance of excitatory over inhibitory processes, it seems reasonable that mutations in genes encoding sodium and potassium channels, as well as glutamatergic and gamma-aminobutyric (GABA) receptors, play a role in the pathogenesis of epilepsy. In some cases, different pathogenic variants of the same gene can result in opposite functional effects, determining the effectiveness of therapy with certain medications. For instance, seizures related to gain-of-function (GoF) mutations in genes encoding sodium channels can be successfully treated with sodium channel blockers. On the contrary, the same drugs may aggravate seizures related to loss-of-function (LoF) variants of the same genes. Hence, knowledge of gene mutation–treatment response relationships facilitates more favorable selection of drugs for anticonvulsant therapy. Full article
(This article belongs to the Special Issue Molecular Research in Epilepsy and Epileptogenesis)
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