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Brain Sciences
Special Issues
Synaptic Changes in Epilepsy
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Synaptic Changes in 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 (25 March 2020) | Viewed by 7071

Special Issue Editor

Prof. Dr. Timo Kirschstein

E-Mail Website
Guest Editor
Institute of Physiology and Department of Neurology, University Medicine Rostock, Germany
Interests: glutamate receptor; GABA receptor; synaptic plasticity; interneuron; glioneural synapse

Special Issue Information

Dear Colleagues,

Research on the pathophysiology of epilepsy has focused on persistent intrinsic changes in excitability using various models of experimental epilepsy and also on human tissue from epilepsy surgery. In these studies, the altered transcription of Na+, Ca2+, or K+ channels was described in epileptic tissue and these were referred to as acquired channelopathies. In recent years, more attention has been drawn to neuronal networks affected by disease in tissues such as the hippocampus. It is well established that pathological axon sprouting gives rise to new synapses with uncommon properties in epileptic tissues. However, we now know that also glutamate and GABA receptors may persistently be altered and further transmitter receptors are increasingly being studied. Thus, elucidating epileptic synaptopathy adds significantly to our pathophysiological understanding of seizure initiation and disease progression during epileptogenesis.

This Special Issue is dedicated to synaptic changes in epilepsy. Studies on interventions to interfere with epilepsy-associated synaptic changes and thus disease-modifying effects are also welcome.

Prof. Dr. Timo Kirschstein
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

  • Synaptic plasticity
  • Glutamate receptors
  • GABA receptors
  • Presynaptic terminal
  • Axon sprouting

Published Papers (2 papers)

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Research

11 pages, 14781 KiB  
Article
Distinct Effects of Stereotactically Injected Human Cerebrospinal Fluid Containing Glutamic Acid Decarboxylase Antibodies into the Hippocampus of Rats on the Development of Spontaneous Epileptic Activity
by Bernd Frerker, Marco Rohde, Steffen Müller, Christian G. Bien, Rüdiger Köhling and Timo Kirschstein
Brain Sci. 2020, 10(2), 123; https://doi.org/10.3390/brainsci10020123 - 22 Feb 2020
Cited by 4 | Viewed by 2941
Abstract
Background: The conversion of glutamic acid into γ-aminobutyric acid (GABA) is catalyzed by the glutamic acid decarboxylase (GAD). Antibodies against this enzyme have been described in neurological disorders, but the pathophysiological role of these antibodies is still poorly understood. We hypothesized that [...] Read more.
Background: The conversion of glutamic acid into γ-aminobutyric acid (GABA) is catalyzed by the glutamic acid decarboxylase (GAD). Antibodies against this enzyme have been described in neurological disorders, but the pathophysiological role of these antibodies is still poorly understood. We hypothesized that anti-GAD autoantibodies could diminish the GABA content in the slice and facilitate epileptic activity. Methods: Cerebrospinal fluids (CSF) from two patients containing anti-GAD (A and B) were injected into the rat hippocampus in vivo. Hippocampal slices were prepared for electrophysiological field potential recordings in order to record recurrent epileptic discharges (REDs) in the CA1 region induced by the removal of Mg2+ and/or by adding gabazine. As control groups, we injected an anti-GAD-negative human CSF or saline solution, and we used non-operated naive animals. Results: RED frequencies were significantly higher in the Mg2+-free solution than in the gabazine-containing solution. The average frequency of REDs in the last 10 min and the average duration of REDs in the last 5 min did not show significant differences between the anti-GAD-B-treated and the control slices, but in the Mg2+-free solution, anti-GAD-A had significantly higher epileptic activity than anti-GAD-B. Conclusions: These results indicate that anti-GAD has distinct effects on the development of spontaneous epileptic activity. Full article
(This article belongs to the Special Issue Synaptic Changes in Epilepsy)
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18 pages, 2419 KiB  
Article
Downregulation of Astrocytic Kir4.1 Potassium Channels Is Associated with Hippocampal Neuronal Hyperexcitability in Type 2 Diabetic Mice
by Miguel P. Méndez-González, David E. Rivera-Aponte, Jan Benedikt, Geronimo Maldonado-Martínez, Flavia Tejeda-Bayron, Serguei N. Skatchkov and Misty J. Eaton
Brain Sci. 2020, 10(2), 72; https://doi.org/10.3390/brainsci10020072 - 30 Jan 2020
Cited by 12 | Viewed by 3763
Abstract
Epilepsy, characterized by recurrent seizures, affects 1% of the general population. Interestingly, 25% of diabetics develop seizures with a yet unknown mechanism. Hyperglycemia downregulates inwardly rectifying potassium channel 4.1 (Kir4.1) in cultured astrocytes. Therefore, the present study aims to determine if downregulation of [...] Read more.
Epilepsy, characterized by recurrent seizures, affects 1% of the general population. Interestingly, 25% of diabetics develop seizures with a yet unknown mechanism. Hyperglycemia downregulates inwardly rectifying potassium channel 4.1 (Kir4.1) in cultured astrocytes. Therefore, the present study aims to determine if downregulation of functional astrocytic Kir4.1 channels occurs in brains of type 2 diabetic mice and could influence hippocampal neuronal hyperexcitability. Using whole-cell patch clamp recording in hippocampal brain slices from male mice, we determined the electrophysiological properties of stratum radiatum astrocytes and CA1 pyramidal neurons. In diabetic mice, astrocytic Kir4.1 channels were functionally downregulated as evidenced by multiple characteristics including depolarized membrane potential, reduced barium-sensitive Kir currents and impaired potassium uptake capabilities of hippocampal astrocytes. Furthermore, CA1 pyramidal neurons from diabetic mice displayed increased spontaneous activity: action potential frequency was ≈9 times higher in diabetic compared with non-diabetic mice and small EPSC event frequency was significantly higher in CA1 pyramidal cells of diabetics compared to non-diabetics. These differences were apparent in control conditions and largely pronounced in response to the pro-convulsant 4-aminopyridine. Our data suggest that astrocytic dysfunction due to downregulation of Kir4.1 channels may increase seizure susceptibility by impairing astrocytic ability to maintain proper extracellular homeostasis. Full article
(This article belongs to the Special Issue Synaptic Changes in Epilepsy)
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