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Diagnostics
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State-of-the-Art Research on Epilepsy
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State-of-the-Art Research on Epilepsy

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Pathology and Molecular Diagnostics".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6786

Special Issue Editors

Prof. Dr. Inga Poletaeva

E-Mail Website
Guest Editor
Biology Department, Lomonosov Moscow State University, Moscow, Russia
Interests: behavior genetics; neurogenetics; physiological foundations of cognitive behavior; audiogenic epilepsy; epileptogenesis; neurogenesis of the adult brain
Dr. Natalia Surina

E-Mail Website
Guest Editor
Biology Department, Lomonosov Moscow State University, Moscow, Russia
Interests: audiogenic epilepsy; behavior genetics; Krushinsky-Molodkina rats; catalepsy; depression; anxiety; behavior; neuroinflammation

Special Issue Information

Dear Colleagues,

Epilepsy is a network disorder accompanied by severe metabolic violations. It affects approximately 1% of the worldwide population. The complexity of epileptogenesis requires intense interdisciplinary research using a variety of models, such as in silico, in vitro and in vivo. Recently, simple models of acute seizures, such as the maximal electroshock seizure test or the pentylenetetrazole seizure test, were used as the standard procedure for predicting clinical anticonvulsant activity for many drug candidates. Next, the kindling models and genetic models were developed, and they helped to overcome serious problems such as false-positive and false-negative evaluations of drug candidates.

In the majority of patients, seizures can be well-controlled when provided with adequately selected therapy. Nevertheless, current medications still fail to eradicate seizures in 30-40% of patients (so called pharmacoresistant epilepsy). Uncontrollable seizure episodes have a significant negative impact on patients’ quality of life, interfering with memory, cognition, comorbid depressive states and anxious disorders. This mediates the necessity of novel approaches and the analysis of seizure states in various models.

We encourage the submission of original research, case reports and review articles on behavioral, electrophysiological, molecular, bioinformatic and cellular pathology, involved in epileptogenesis.

Prof. Dr. Inga Poletaeva
Dr. Natalia Surina
Guest Editors

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. Diagnostics is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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
  • animal models
  • epileptogenesis
  • reflex seizures
  • genetics
  • comorbid disorders
  • kindling
  • secondary epileptogenesis
  • antiepileptic drugs
  • therapy response prediction
  • EEG

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Published Papers (3 papers)

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Research

28 pages, 3665 KiB  
Article
Proteomic and Bioinformatic Tools to Identify Potential Hub Proteins in the Audiogenic Seizure-Prone Hamster GASH/Sal
by Carlos García-Peral, Martín M. Ledesma, M. Javier Herrero-Turrión, Ricardo Gómez-Nieto, Orlando Castellano and Dolores E. López
Diagnostics 2023, 13(6), 1048; https://doi.org/10.3390/diagnostics13061048 - 9 Mar 2023
Cited by 3 | Viewed by 2381
Abstract
The GASH/Sal (Genetic Audiogenic Seizure Hamster, Salamanca) is a model of audiogenic seizures with the epileptogenic focus localized in the inferior colliculus (IC). The sound-induced seizures exhibit a short latency (7–9 s), which implies innate protein disturbances in the IC as a basis [...] Read more.
The GASH/Sal (Genetic Audiogenic Seizure Hamster, Salamanca) is a model of audiogenic seizures with the epileptogenic focus localized in the inferior colliculus (IC). The sound-induced seizures exhibit a short latency (7–9 s), which implies innate protein disturbances in the IC as a basis for seizure susceptibility and generation. Here, we aim to study the protein profile in the GASH/Sal IC in comparison to controls. Protein samples from the IC were processed for enzymatic digestion and then analyzed by mass spectrometry in Data-Independent Acquisition mode. After identifying the proteins using the UniProt database, we selected those with differential expression and performed ontological analyses, as well as gene-protein interaction studies using bioinformatics tools. We identified 5254 proteins; among them, 184 were differentially expressed proteins (DEPs), with 126 upregulated and 58 downregulated proteins, and 10 of the DEPs directly related to epilepsy. Moreover, 12 and 7 proteins were uniquely found in the GASH/Sal or the control. The results indicated a protein profile alteration in the epileptogenic nucleus that might underlie the inborn occurring audiogenic seizures in the GASH/Sal model. In summary, this study supports the use of bioinformatics methods in proteomics to delve into the relationship between molecular-level protein mechanisms and the pathobiology of rodent models of audiogenic seizures. Full article
(This article belongs to the Special Issue State-of-the-Art Research on Epilepsy)
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14 pages, 5149 KiB  
Article
Striatal Patchwork of D1-like and D2-like Receptors Binding Densities in Rats with Genetic Audiogenic and Absence Epilepsies
by Evgeniya T. Tsyba, Inna S. Midzyanovskaya, Lidia M. Birioukova, Leena M. Tuomisto, Gilles van Luijtelaar and Kenul R. Abbasova
Diagnostics 2023, 13(4), 587; https://doi.org/10.3390/diagnostics13040587 - 5 Feb 2023
Cited by 6 | Viewed by 1576
Abstract
Binding densities to dopamine D1-like and D2-like receptors (D1DR and D2DR) were studied in brain regions of animals with genetic generalized audiogenic (AGS) and/or absence (AbS) epilepsy (KM, WAG/Rij-AGS, and WAG/Rij rats, respectively) as compared to non-epileptic Wistar (WS) rats. Convulsive epilepsy (AGS) [...] Read more.
Binding densities to dopamine D1-like and D2-like receptors (D1DR and D2DR) were studied in brain regions of animals with genetic generalized audiogenic (AGS) and/or absence (AbS) epilepsy (KM, WAG/Rij-AGS, and WAG/Rij rats, respectively) as compared to non-epileptic Wistar (WS) rats. Convulsive epilepsy (AGS) exerted a major effect on the striatal subregional binding densities for D1DR and D2DR. An increased binding density to D1DR was found in the dorsal striatal subregions of AGS-prone rats. Similar changes were seen for D2DR in the central and dorsal striatal territories. Subregions of the nucleus accumbens demonstrated consistent subregional decreases in the binding densities of D1DR and D2DR in epileptic animals, irrespective of epilepsy types. This was seen for D1DR in the dorsal core, dorsal, and ventrolateral shell; and for D2DR in the dorsal, dorsolateral, and ventrolateral shell. An increased density of D2DR was found in the motor cortex of AGS-prone rats. An AGS-related increase in binding densities to D1DR and D2DR in the dorsal striatum and motor cortex, areas responsible for motor activity, possibly reflects the activation of brain anticonvulsive loops. General epilepsy-related decreases in binding densities to D1DR and D2DR in the accumbal subregions might contribute to behavioral comorbidities of epilepsy. Full article
(This article belongs to the Special Issue State-of-the-Art Research on Epilepsy)
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16 pages, 1825 KiB  
Article
Maternal Methyl-Enriched Diet Increases DNMT1, HCN1, and TH Gene Expression and Suppresses Absence Seizures and Comorbid Depression in Offspring of WAG/Rij Rats
by Karine Yu. Sarkisova, Ekaterina A. Fedosova, Alla B. Shatskova, Margarita M. Rudenok, Vera A. Stanishevskaya and Petr A. Slominsky
Diagnostics 2023, 13(3), 398; https://doi.org/10.3390/diagnostics13030398 - 21 Jan 2023
Cited by 8 | Viewed by 1984
Abstract
The reduced expression of the HCN1 ion channel in the somatosensory cortex (SSC) and mesolimbic dopamine deficiency are thought to be associated with the genesis of spike-wave discharges (SWDs) and comorbid depression in the WAG/Rij rat model of absence epilepsy. This study aimed [...] Read more.
The reduced expression of the HCN1 ion channel in the somatosensory cortex (SSC) and mesolimbic dopamine deficiency are thought to be associated with the genesis of spike-wave discharges (SWDs) and comorbid depression in the WAG/Rij rat model of absence epilepsy. This study aimed to investigate whether the maternal methyl-enriched diet (MED), which affects DNA methylation, can alter DNMT1, HCN1, and TH gene expression and modify absence seizures and comorbid depression in WAG/Rij offspring. WAG/Rij mothers were fed MED (choline, betaine, folic acid, vitamin B12, L-methionine, zinc) or a control diet for a week before mating, during pregnancy, and for a week after parturition. MED caused sustained suppression of SWDs and symptoms of comorbid depression in the offspring. Disease-modifying effects of MED were associated with increased expression of the DNMT1 and HCN1 genes in the SSC and hippocampus, as well as DNMT1, HCN1, and TH genes in the nucleus accumbens. No changes in gene expression were detected in the hypothalamus. The results indicate that maternal MED can suppress the genetic absence epilepsy and comorbid depression in offspring. Increased expression of the DNMT1, HCN1, and TH genes is suggested to be a molecular mechanism of this beneficial phenotypic effect. Full article
(This article belongs to the Special Issue State-of-the-Art Research on Epilepsy)
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