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Brain Sciences
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The Molecular and Cellular Mechanisms of Epilepsy
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The Molecular and Cellular Mechanisms of Epilepsy

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 8787

Special Issue Editors

Dr. Aleksey Zaitsev

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Guest Editor
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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Roustem Khazipov

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Co-Guest Editor
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 Issues, Collections and Topics in MDPI journals

Special Issue Information

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, The Molecular and Cellular Mechanisms of Epilepsy”, of Brain Sciences 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
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. Brain Sciences is an international peer-reviewed open access monthly 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 2200 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
  • epilepsy models
  • epileptogenesis
  • preventing epilepsy
  • neuroinflammation
  • neuroprotection
  • synaptic plasticity
  • neuron–astrocyte interaction

Published Papers (3 papers)

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Research

13 pages, 3829 KiB  
Article
In Vitro and In Vivo Study of the Short-Term Vasomotor Response during Epileptic Seizures
by Anna Volnova, Vassiliy Tsytsarev, Maria Ptukha and Mikhail Inyushin
Brain Sci. 2020, 10(12), 942; https://doi.org/10.3390/brainsci10120942 - 7 Dec 2020
Cited by 7 | Viewed by 2303
Abstract
Epilepsy remains one of the most common brain disorders, and the different types of epilepsy encompass a wide variety of physiological manifestations. Clinical and preclinical findings indicate that cerebral blood flow is usually focally increased at seizure onset, shortly after the beginning of [...] Read more.
Epilepsy remains one of the most common brain disorders, and the different types of epilepsy encompass a wide variety of physiological manifestations. Clinical and preclinical findings indicate that cerebral blood flow is usually focally increased at seizure onset, shortly after the beginning of ictal events. Nevertheless, many questions remain about the relationship between vasomotor changes in the epileptic foci and the epileptic behavior of neurons and astrocytes. To study this relationship, we performed a series of in vitro and in vivo experiments using the 4-aminopyridine model of epileptic seizures. It was found that in vitro pathological synchronization of neurons and the depolarization of astrocytes is accompanied by rapid short-term vasoconstriction, while in vivo vasodilation during the seizure prevails. We suggest that vasomotor activity during epileptic seizures is a correlate of the complex, self-sustained response that includes neuronal and astrocytic oscillations, and that underlies the clinical presentation of epilepsy. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Epilepsy)
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20 pages, 4380 KiB  
Article
A Translational Study on Acute Traumatic Brain Injury: High Incidence of Epileptiform Activity on Human and Rat Electrocorticograms and Histological Correlates in Rats
by Ilia G. Komoltsev, Mikhail V. Sinkin, Aleksandra A. Volkova, Elizaveta A. Smirnova, Margarita R. Novikova, Olga O. Kordonskaya, Alexander E. Talypov, Alla B. Guekht, Vladimir V. Krylov and Natalia V. Gulyaeva
Brain Sci. 2020, 10(9), 570; https://doi.org/10.3390/brainsci10090570 - 19 Aug 2020
Cited by 8 | Viewed by 3452
Abstract
Background: In humans, early pathological activity on invasive electrocorticograms (ECoGs) and its putative association with pathomorphology in the early period of traumatic brain injury (TBI) remains obscure. Methods: We assessed pathological activity on scalp electroencephalograms (EEGs) and ECoGs in patients with acute TBI, [...] Read more.
Background: In humans, early pathological activity on invasive electrocorticograms (ECoGs) and its putative association with pathomorphology in the early period of traumatic brain injury (TBI) remains obscure. Methods: We assessed pathological activity on scalp electroencephalograms (EEGs) and ECoGs in patients with acute TBI, early electrophysiological changes after lateral fluid percussion brain injury (FPI), and electrophysiological correlates of hippocampal damage (microgliosis and neuronal loss), a week after TBI in rats. Results: Epileptiform activity on ECoGs was evident in 86% of patients during the acute period of TBI, ECoGs being more sensitive to epileptiform and periodic discharges. A “brush-like” ECoG pattern superimposed over rhythmic delta activity and periodic discharge was described for the first time in acute TBI. In rats, FPI increased high-amplitude spike incidence in the neocortex and, most expressed, in the ipsilateral hippocampus, induced hippocampal microgliosis and neuronal loss, ipsilateral dentate gyrus being most vulnerable, a week after TBI. Epileptiform spike incidence correlated with microglial cell density and neuronal loss in the ipsilateral hippocampus. Conclusion: Epileptiform activity is frequent in the acute period of TBI period and is associated with distant hippocampal damage on a microscopic level. This damage is probably involved in late consequences of TBI. The FPI model is suitable for exploring pathogenetic mechanisms of post-traumatic disorders. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Epilepsy)
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15 pages, 4630 KiB  
Article
Glutamatergic Fate of Neural Progenitor Cells of Rats with Inherited Audiogenic Epilepsy
by Alexandra A. Naumova, Ekaterina A. Oleynik, Elena V. Chernigovskaya and Margarita V. Glazova
Brain Sci. 2020, 10(5), 311; https://doi.org/10.3390/brainsci10050311 - 21 May 2020
Cited by 5 | Viewed by 2589
Abstract
Epilepsy is associated with aberrant neurogenesis in the hippocampus and may underlie the development of hereditary epilepsy. In the present study, we analyzed the differentiation fate of neural progenitor cells (NPC), which were isolated from the hippocampus of embryos of Krushinsky-Molodkina (KM) rats [...] Read more.
Epilepsy is associated with aberrant neurogenesis in the hippocampus and may underlie the development of hereditary epilepsy. In the present study, we analyzed the differentiation fate of neural progenitor cells (NPC), which were isolated from the hippocampus of embryos of Krushinsky-Molodkina (KM) rats genetically prone to audiogenic epilepsy. NPCs from embryos of Wistar rats were used as the control. We found principal differences between Wistar and KM NPC in unstimulated controls: Wistar NPC culture contained both gamma-aminobutyric acid (GABA) and glutamatergic neurons; KM NPC culture was mainly represented by glutamatergic cells. The stimulation of glutamatergic differentiation of Wistar NPC resulted in a significant increase in glutamatergic cell number that was accompanied by the activation of protein kinase A. The stimulation of KM NPC led to a decrease in immature glutamatergic cell number and was associated with the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and protein kinase B/ glycogen synthase kinase 3 beta (Akt/GSK3β), which indicates the activation of glutamatergic cell maturation. These results suggest genetically programmed abnormalities in KM rats that determine the glutamatergic fate of NPC and contribute to the development of audiogenic epilepsy. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Epilepsy)
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