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Molecular and Cellular Mechanisms of Epilepsy—3rd Edition
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Molecular and Cellular Mechanisms of Epilepsy—3rd Edition

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: 20 November 2024 | Viewed by 8572

Special Issue Editor

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

Special Issue Information

Dear Colleagues,

This is a continued collection of the hot topic on Epilepsy. We already have done two successful special issues which received interesting contributions and discussions (https://www.mdpi.com/journal/ijms/special_issues/molecular_cellular_epilepsy; https://www.mdpi.com/journal/ijms/special_issues/KLPQB5U741).

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 3.0”, 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

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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.

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Keywords

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

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Published Papers (5 papers)

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Research

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17 pages, 7138 KiB  
Article
Metabolic Adaptation in Epilepsy: From Acute Response to Chronic Impairment
by Agustin Liotta, Stefan Loroch, Iwona Wallach, Kristoffer Klewe, Katrin Marcus and Nikolaus Berndt
Int. J. Mol. Sci. 2024, 25(17), 9640; https://doi.org/10.3390/ijms25179640 - 6 Sep 2024
Viewed by 659
Abstract
Epilepsy is characterized by hypersynchronous neuronal discharges, which are associated with an increased cerebral metabolic rate of oxygen and ATP demand. Uncontrolled seizure activity (status epilepticus) results in mitochondrial exhaustion and ATP depletion, which potentially generate energy mismatch and neuronal loss. Many cells [...] Read more.
Epilepsy is characterized by hypersynchronous neuronal discharges, which are associated with an increased cerebral metabolic rate of oxygen and ATP demand. Uncontrolled seizure activity (status epilepticus) results in mitochondrial exhaustion and ATP depletion, which potentially generate energy mismatch and neuronal loss. Many cells can adapt to increased energy demand by increasing metabolic capacities. However, acute metabolic adaptation during epileptic activity and its relationship to chronic epilepsy remains poorly understood. We elicited seizure-like events (SLEs) in an in vitro model of status epilepticus for eight hours. Electrophysiological recording and tissue oxygen partial pressure recordings were performed. After eight hours of ongoing SLEs, we used proteomics-based kinetic modeling to evaluate changes in metabolic capacities. We compared our findings regarding acute metabolic adaptation to published proteomic and transcriptomic data from chronic epilepsy patients. Epileptic tissue acutely responded to uninterrupted SLEs by upregulating ATP production capacity. This was achieved by a coordinated increase in the abundance of proteins from the respiratory chain and oxidative phosphorylation system. In contrast, chronic epileptic tissue shows a 25–40% decrease in ATP production capacity. In summary, our study reveals that epilepsy leads to dynamic metabolic changes. Acute epileptic activity boosts ATP production, while chronic epilepsy reduces it significantly. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy—3rd Edition)
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21 pages, 6982 KiB  
Article
Morphological and Functional Alterations in the CA1 Pyramidal Neurons of the Rat Hippocampus in the Chronic Phase of the Lithium–Pilocarpine Model of Epilepsy
by Tatyana Y. Postnikova, Georgy P. Diespirov, Sergey L. Malkin, Alexander S. Chernyshev, Elizaveta N. Vylekzhanina and Aleksey V. Zaitsev
Int. J. Mol. Sci. 2024, 25(14), 7568; https://doi.org/10.3390/ijms25147568 - 10 Jul 2024
Viewed by 964
Abstract
Epilepsy is known to cause alterations in neural networks. However, many details of these changes remain poorly understood. The objective of this study was to investigate changes in the properties of hippocampal CA1 pyramidal neurons and their synaptic inputs in a rat lithium–pilocarpine [...] Read more.
Epilepsy is known to cause alterations in neural networks. However, many details of these changes remain poorly understood. The objective of this study was to investigate changes in the properties of hippocampal CA1 pyramidal neurons and their synaptic inputs in a rat lithium–pilocarpine model of epilepsy. In the chronic phase of the model, we found a marked loss of pyramidal neurons in the CA1 area. However, the membrane properties of the neurons remained essentially unaltered. The results of the electrophysiological and morphological studies indicate that the direct pathway from the entorhinal cortex to CA1 neurons is reinforced in epileptic animals, whereas the inputs to them from CA3 are either unaltered or even diminished. In particular, the dendritic spine density in the str. lacunosum moleculare, where the direct pathway from the entorhinal cortex terminates, was found to be 2.5 times higher in epileptic rats than in control rats. Furthermore, the summation of responses upon stimulation of the temporoammonic pathway was enhanced by approximately twofold in epileptic rats. This enhancement is believed to be a significant contributing factor to the heightened epileptic activity observed in the entorhinal cortex of epileptic rats using an ex vivo 4-aminopyridine model. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy—3rd Edition)
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19 pages, 2068 KiB  
Article
Dissimilar Changes in Serum Cortisol after Epileptic and Psychogenic Non-Epileptic Seizures: A Promising Biomarker in the Differential Diagnosis of Paroxysmal Events?
by Flora Rider, Alexander Turchinets, Tatyana Druzhkova, Georgii Kustov, Alla Guekht and Natalia Gulyaeva
Int. J. Mol. Sci. 2024, 25(13), 7387; https://doi.org/10.3390/ijms25137387 - 5 Jul 2024
Viewed by 1142
Abstract
The hypothalamic–pituitary–adrenal axis is known to be involved in the pathogenesis of epilepsy and psychiatric disorders. Epileptic seizures (ESs) and psychogenic non-epileptic seizures (PNESs) are frequently differentially misdiagnosed. This study aimed to evaluate changes in serum cortisol and prolactin levels after ESs and [...] Read more.
The hypothalamic–pituitary–adrenal axis is known to be involved in the pathogenesis of epilepsy and psychiatric disorders. Epileptic seizures (ESs) and psychogenic non-epileptic seizures (PNESs) are frequently differentially misdiagnosed. This study aimed to evaluate changes in serum cortisol and prolactin levels after ESs and PNESs as possible differential diagnostic biomarkers. Patients over 18 years with ESs (n = 29) and PNESs with motor manifestations (n = 45), captured on video-EEG monitoring, were included. Serum cortisol and prolactin levels as well as hemograms were assessed in blood samples taken at admission, during the first hour after the seizure, and after 6, 12, and 24 h. Cortisol and prolactine response were evident in the ES group (but not the PNES group) as an acute significant increase within the first hour after seizure. The occurrence of seizures in patients with ESs and PNESs demonstrated different circadian patterns. ROC analysis confirmed the accuracy of discrimination between paroxysmal events based on cortisol response: the AUC equals 0.865, with a prediction accuracy at the cutoff point of 376.5 nmol/L 0.811 (sensitivity 86.7%, specificity 72.4%). Thus, assessments of acute serum cortisol response to a paroxysmal event may be regarded as a simple, fast, and minimally invasive laboratory test contributing to differential diagnosis of ESs and PNESs. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy—3rd Edition)
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12 pages, 1749 KiB  
Article
Matrix Metalloproteinase-9 Contributes to Epilepsy Development after Ischemic Stroke in Mice
by Barbara Pijet, Agnieszka Kostrzewska-Księzyk, Maja Pijet-Kucicka and Leszek Kaczmarek
Int. J. Mol. Sci. 2024, 25(2), 896; https://doi.org/10.3390/ijms25020896 - 11 Jan 2024
Cited by 1 | Viewed by 1219
Abstract
Epilepsy, a neurological disorder affecting over 50 million individuals globally, is characterized by an enduring predisposition and diverse consequences, both neurobiological and social. Acquired epilepsy, constituting 30% of cases, often results from brain-damaging injuries like ischemic stroke. With one third of epilepsy cases [...] Read more.
Epilepsy, a neurological disorder affecting over 50 million individuals globally, is characterized by an enduring predisposition and diverse consequences, both neurobiological and social. Acquired epilepsy, constituting 30% of cases, often results from brain-damaging injuries like ischemic stroke. With one third of epilepsy cases being resistant to existing drugs and without any preventive therapeutics for epileptogenesis, identifying anti-epileptogenic targets is crucial. Stroke being a leading cause of acquired epilepsy, particularly in the elderly, prompts the need for understanding post-stroke epileptogenesis. Despite the challenges in studying stroke-evoked epilepsy in rodents due to poor long-term survival rates, in this presented study the use of an animal care protocol allowed for comprehensive investigation. We highlight the role of matrix metalloproteinase-9 (MMP-9) in post-stroke epileptogenesis, emphasizing MMP-9 involvement in mouse models and its potential as a therapeutic target. Using a focal Middle Cerebral Artery occlusion model, this study demonstrates MMP-9 activation following ischemia, influencing susceptibility to seizures. MMP-9 knockout reduces epileptic features, while overexpression exacerbates them. The findings show that MMP-9 is a key player in post-stroke epileptogenesis, presenting opportunities for future therapies and expanding our understanding of acquired epilepsy. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy—3rd Edition)
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Review

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40 pages, 2520 KiB  
Review
Virus-Induced Epilepsy vs. Epilepsy Patients Acquiring Viral Infection: Unravelling the Complex Relationship for Precision Treatment
by Bárbara Costa and Nuno Vale
Int. J. Mol. Sci. 2024, 25(7), 3730; https://doi.org/10.3390/ijms25073730 - 27 Mar 2024
Cited by 2 | Viewed by 3863
Abstract
The intricate relationship between viruses and epilepsy involves a bidirectional interaction. Certain viruses can induce epilepsy by infecting the brain, leading to inflammation, damage, or abnormal electrical activity. Conversely, epilepsy patients may be more susceptible to viral infections due to factors, such as [...] Read more.
The intricate relationship between viruses and epilepsy involves a bidirectional interaction. Certain viruses can induce epilepsy by infecting the brain, leading to inflammation, damage, or abnormal electrical activity. Conversely, epilepsy patients may be more susceptible to viral infections due to factors, such as compromised immune systems, anticonvulsant drugs, or surgical interventions. Neuroinflammation, a common factor in both scenarios, exhibits onset, duration, intensity, and consequence variations. It can modulate epileptogenesis, increase seizure susceptibility, and impact anticonvulsant drug pharmacokinetics, immune system function, and brain physiology. Viral infections significantly impact the clinical management of epilepsy patients, necessitating a multidisciplinary approach encompassing diagnosis, prevention, and treatment of both conditions. We delved into the dual dynamics of viruses inducing epilepsy and epilepsy patients acquiring viruses, examining the unique features of each case. For virus-induced epilepsy, we specify virus types, elucidate mechanisms of epilepsy induction, emphasize neuroinflammation’s impact, and analyze its effects on anticonvulsant drug pharmacokinetics. Conversely, in epilepsy patients acquiring viruses, we detail the acquired virus, its interaction with existing epilepsy, neuroinflammation effects, and changes in anticonvulsant drug pharmacokinetics. Understanding this interplay advances precision therapies for epilepsy during viral infections, providing mechanistic insights, identifying biomarkers and therapeutic targets, and supporting optimized dosing regimens. However, further studies are crucial to validate tools, discover new biomarkers and therapeutic targets, and evaluate targeted therapy safety and efficacy in diverse epilepsy and viral infection scenarios. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Epilepsy—3rd Edition)
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