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Methionine Sulfoximine as a Tool for Studying Temporal Lobe Epilepsy: Initiator, Developer, Attenuator.
Neurochem Res
January 2025
Department of Pathophysiology, Medical University of Lublin, 20-090, Lublin, Poland.
Methionine sulfoximine (MSO) is a compound originally discovered as a byproduct of agene-based milled flour maturation. MSO irreversibly inhibits the astrocytic enzyme glutamine synthase (GS) but also interferes with the transport of glutamine (Gln) and of glutamate (Glu), and γ-aminobutyric acid (GABA) synthesized within the Glu/Gln-GABA cycle, in this way dysregulating neurotransmission balance in favor of excitation. No wonder that intraperitoneal administration of MSO has long been known to induce behavioral and/or electrographic seizures.
View Article and Find Full Text PDFAltered Hippocampal Activation in Seizure-Prone Knock-out Mice.
eNeuro
May 2024
Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, Oregon 97239
The voltage-gated calcium channel subunit α2δ-2 controls calcium-dependent signaling in neurons, and loss of this subunit causes epilepsy in both mice and humans. To determine whether mice without α2δ-2 demonstrate hippocampal activation or histopathological changes associated with seizure activity, we measured expression of the activity-dependent gene c and various histopathological correlates of temporal lobe epilepsy (TLE) in hippocampal tissue from wild-type (WT) and α2δ-2 knock-out ( KO) mice using immunohistochemical staining and confocal microscopy. Both genotypes demonstrated similarly sparse c- and expressions within the hippocampal dentate granule cell layer (GCL) at baseline, consistent with no difference in basal activity of granule cells between genotypes.
View Article and Find Full Text PDFMiR129-5p-loaded exosomes suppress seizure-associated neurodegeneration in status epilepticus model mice by inhibiting HMGB1/TLR4-mediated neuroinflammation.
Mol Biol Rep
February 2024
Department of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, Jiangsu, China.
Background: Neuroinflammation contributes to both epileptogenesis and the associated neurodegeneration, so regulation of inflammatory signaling is a potential strategy for suppressing epilepsy development and pathological progression. Exosomes are enriched in microRNAs (miRNAs), considered as vital communication tools between cells, which have been proven as potential therapeutic method for neurological disease. Here, we investigated the role of miR129-5p-loaded mesenchymal stem cell (MSC)-derived exosomes in status epilepticus (SE) mice model.
View Article and Find Full Text PDFAltered hippocampal activation in seizure-prone knockout mice.
bioRxiv
November 2023
Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, 97239.
Article Synopsis
- * Even though knockout (KO) mice showed fewer active cells in the dentate gyrus after handling-induced seizures, they exhibited increased activation when given a low dose of a seizure-inducing drug compared to wildtype (WT) mice, indicating heightened sensitivity to convulsions.
- * Histopathological markers, such as neurogenesis and glial activation, were largely similar in both KO and WT mice, except for a notable increase in hilar mossy cell density in KO mice,
Reduced Cholecystokinin-Expressing Interneuron Input Contributes to Disinhibition of the Hippocampal CA2 Region in a Mouse Model of Temporal Lobe Epilepsy.
J Neurosci
October 2023
Departments of Neuroscience and Pharmacology, Kavli Institute for Brain Science, Mortimer B. Zuckerman Mind Brain Behavior Institute, Columbia University Irving Medical Center, New York, New York 10027
A significant proportion of temporal lobe epilepsy (TLE) patients experience drug-resistant seizures associated with mesial temporal sclerosis, in which there is extensive cell loss in the hippocampal CA1 and CA3 subfields, with a relative sparing of dentate gyrus granule cells and CA2 pyramidal neurons (PNs). A role for CA2 in seizure generation was suggested based on findings of a reduction in CA2 synaptic inhibition (Williamson and Spencer, 1994) and the presence of interictal-like spike activity in CA2 in resected hippocampal tissue from TLE patients (Wittner et al., 2009).
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