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Neuronal, Glial, and Immune Changes in Models of Epilepsy and Epileptogenesis-2nd 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: closed (30 April 2022) | Viewed by 10239

Special Issue Editor

Prof. Dr. Lee A. Shapiro

E-Mail Website
Guest Editor
Department of Surgery, Texas A & M University Health Science Center, College of Medicine, Temple, TX 76504, USA
Interests: neuroscience; neurodegenerative disorders; neuroimmune
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epilepsy is one of the most common neurological disorders and affects people of all ages and genders. Epilepsy is defined as the recurrent appearance of seizures, and these seizures can be highly variable among individuals. Some types of epilepsy have predisposing, underlying factors, whereas others can be the result of injury or insult. Common themes in the development of epilepsy are changes to cellular, genetic, immune, anatomical, molecular, and physiological mechanisms, which ultimately result in the appearance of seizures and/or an increase in seizure susceptibility. This process of epileptogenesis can be highly unpredictable with regard to the timing, triggers, and specific mechanisms involved. Neurons and glial cells make up the fundamental cellular components of the central nervous system. The dysfunction of these cell types and the circuits to which they contribute can be pro-epileptogenic. A growing body of evidence also implicates inflammatory and neuroinflammatory mechanisms, as well as genetic and epigenetic factors in the development of epilepsy. Here, we seek manuscripts and review articles that pertain to cellular and immune contributions to seizures, epileptogenic progression, and the development of epilepsy. Studies that incorporate wide-ranging models, including injury models, are encouraged.

Prof. Dr. Lee A. Shapiro
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
  • Epileptogenesis
  • Seizure
  • Traumatic brain injury
  • Post-traumatic epilepsy
  • Injury
  • Neurons
  • Glia
  • Astrocyte
  • Microglia
  • Inflammation
  • Neuroinflammation
  • Cytokines
  • Immune
  • Neuroimmune
  • Neuroimmunity
  • B-cells
  • T-cells
  • Macrophage
  • Lymphocyte
  • Hyperexcitable

Published Papers (3 papers)

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Research

17 pages, 8353 KiB  
Article
Neurons Induce Tiled Astrocytes with Branches That Avoid Each Other
by Mariko Kato Hayashi, Kaoru Sato and Yuko Sekino
Int. J. Mol. Sci. 2022, 23(8), 4161; https://doi.org/10.3390/ijms23084161 - 9 Apr 2022
Cited by 2 | Viewed by 4373
Abstract
Neurons induce astrocyte branches that approach synapses. Each astrocyte tiles by expanding branches in an exclusive territory, with limited entries for the neighboring astrocyte branches. However, how astrocytes form exclusive territories is not known. For example, the extensive branching of astrocytes may sterically [...] Read more.
Neurons induce astrocyte branches that approach synapses. Each astrocyte tiles by expanding branches in an exclusive territory, with limited entries for the neighboring astrocyte branches. However, how astrocytes form exclusive territories is not known. For example, the extensive branching of astrocytes may sterically interfere with the penetration of other astrocyte branches. Alternatively, astrocyte branches may actively avoid each other or remove overlapped branches to establish a territory. Here, we show time-lapse imaging of the multi-order branching process of GFP-labeled astrocytes. Astrocyte branches grow in the direction where other astrocyte branches do not exist. Neurons that had just started to grow dendrites were able to induce astrocyte branching and tiling. Upon neuronal loss by glutamate excitotoxicity, astrocytes’ terminal processes retracted and more branches went over other branches. Our results indicate that neurons induce astrocyte branches and make them avoid each other. Full article
(This article belongs to the Special Issue Neuronal, Glial, and Immune Changes in Models of Epilepsy and Epileptogenesis-2nd Edition)
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15 pages, 3804 KiB  
Article
Potentiating Hemorrhage in a Periadolescent Rat Model of Closed-Head Traumatic Brain Injury Worsens Hyperexcitability but Not Behavioral Deficits
by Dounya Jalloul, Helene Hajjar, Rita Asdikian, Mariam Maawie, Leila Nasrallah, Yasser Medlej, Mouhamad Darwich, Nabil Karnib, Nada Lawand, Ronza Abdel Rassoul, Kevin K. W. Wang, Firas Kobeissy, Hala Darwish and Makram Obeid
Int. J. Mol. Sci. 2021, 22(12), 6456; https://doi.org/10.3390/ijms22126456 - 16 Jun 2021
Cited by 2 | Viewed by 2809
Abstract
Post-traumatic epilepsy (PTE) and neurocognitive deficits are devastating sequelae of head injuries that are common in adolescents. Investigating desperately needed treatments is hindered by the difficulties in inducing PTE in rodents and the lack of established immature rat models of pediatric PTE. Hemorrhage [...] Read more.
Post-traumatic epilepsy (PTE) and neurocognitive deficits are devastating sequelae of head injuries that are common in adolescents. Investigating desperately needed treatments is hindered by the difficulties in inducing PTE in rodents and the lack of established immature rat models of pediatric PTE. Hemorrhage is a significant risk factor for PTE, but compared to humans, rats are less prone to bleeding because of their rapid blood coagulation system. In this study, we promoted bleeding in the controlled cortical impact (CCI) closed-head injury model with a 20 min pre-impact 600 IU/kg intraperitoneal heparin injection in postnatal day 35 (P35) periadolescent rats, given the preponderance of such injuries in this age group. Temporo-parietal CCI was performed post-heparin (HTBI group) or post-saline (TBI group). Controls were subjected to sham procedures following heparin or saline administration. Continuous long-term EEG monitoring was performed for 3 months post-CCI. Sensorimotor testing, the Morris water maze, and a modified active avoidance test were conducted between P80 and P100. Glial fibrillary acidic protein (GFAP) levels and neuronal damage were also assessed. Compared to TBI rats, HTBI rats had persistently higher EEG spiking and increased hippocampal GFAP levels (p < 0.05). No sensorimotor deficits were detected in any group. Compared to controls, both HTBI and TBI groups had a long-term hippocampal neuronal loss (p < 0.05), as well as contextual and visuospatial learning deficits (p < 0.05). The hippocampal astrogliosis and EEG spiking detected in all rats subjected to our hemorrhage-promoting procedure suggest the emergence of hyperexcitable networks and pave the way to a periadolescent PTE rat model. Full article
(This article belongs to the Special Issue Neuronal, Glial, and Immune Changes in Models of Epilepsy and Epileptogenesis-2nd Edition)
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22 pages, 13629 KiB  
Article
Reorganization of Thalamic Inputs to Lesioned Cortex Following Experimental Traumatic Brain Injury
by Xavier Ekolle Ndode-Ekane, Maria del Mar Puigferrat Pérez, Rossella Di Sapia, Niina Lapinlampi and Asla Pitkänen
Int. J. Mol. Sci. 2021, 22(12), 6329; https://doi.org/10.3390/ijms22126329 - 13 Jun 2021
Cited by 5 | Viewed by 2490
Abstract
Traumatic brain injury (TBI) disrupts thalamic and cortical integrity. The effect of post-injury reorganization and plasticity in thalamocortical pathways on the functional outcome remains unclear. We evaluated whether TBI causes structural changes in the thalamocortical axonal projection terminals in the primary somatosensory cortex [...] Read more.
Traumatic brain injury (TBI) disrupts thalamic and cortical integrity. The effect of post-injury reorganization and plasticity in thalamocortical pathways on the functional outcome remains unclear. We evaluated whether TBI causes structural changes in the thalamocortical axonal projection terminals in the primary somatosensory cortex (S1) that lead to hyperexcitability. TBI was induced in adult male Sprague Dawley rats with lateral fluid-percussion injury. A virus carrying the fluorescent-tagged opsin channel rhodopsin 2 transgene was injected into the ventroposterior thalamus. We then traced the thalamocortical pathways and analyzed the reorganization of their axonal terminals in S1. Next, we optogenetically stimulated the thalamocortical relays from the ventral posterior lateral and medial nuclei to assess the post-TBI functionality of the pathway. Immunohistochemical analysis revealed that TBI did not alter the spatial distribution or lamina-specific targeting of projection terminals in S1. TBI reduced the axon terminal density in the motor cortex by 44% and in S1 by 30%. A nematic tensor-based analysis revealed that in control rats, the axon terminals in layer V were orientated perpendicular to the pial surface (60.3°). In TBI rats their orientation was more parallel to the pial surface (5.43°, difference between the groups p < 0.05). Moreover, the level of anisotropy of the axon terminals was high in controls (0.063) compared with TBI rats (0.045, p < 0.05). Optical stimulation of the sensory thalamus increased alpha activity in electroencephalography by 312% in controls (p > 0.05) and 237% (p > 0.05) in TBI rats compared with the baseline. However, only TBI rats showed increased beta activity (33%) with harmonics at 5 Hz. Our findings indicate that TBI induces reorganization of thalamocortical axonal terminals in the perilesional cortex, which alters responses to thalamic stimulation. Full article
(This article belongs to the Special Issue Neuronal, Glial, and Immune Changes in Models of Epilepsy and Epileptogenesis-2nd Edition)
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