Roles of Very Fast Ripple (500–1000Hz) in the Hippocampal Network During Status Epilepticus

2020 ◽  
pp. 2150002
Author(s):  
Jianmin Hao ◽  
Yan Cui ◽  
Bochao Niu ◽  
Liang Yu ◽  
Yuhang Lin ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Temporal Lobe ◽  
Phase Locking ◽  
Epileptic Seizures ◽  
Network Activity ◽  
Slow Oscillations ◽  
Functional Roles ◽  
High Frequency Oscillations ◽  
Epileptiform Discharges ◽  
Hippocampal Network

Very fast ripples (VFRs, 500–1000[Formula: see text]Hz) are considered more specific than high-frequency oscillations (80–500[Formula: see text]Hz) as biomarkers of epileptogenic zones. Although VFRs are frequent abnormal phenomena in epileptic seizures, their functional roles remain unclear. Here, we detected the VFRs in the hippocampal network and tracked their roles during status epilepticus (SE) in rats with pilocarpine-induced temporal lobe epilepsy (TLE). All regions in the hippocampal network exhibited VFRs in the baseline, preictal, ictal and postictal states, with the ictal state containing the most VFRs. Moreover, strong phase-locking couplings existed between VFRs and slow oscillations (1–12[Formula: see text]Hz) in the ictal and postictal states for all regions. Further investigation indicated that during VFRs, the build-up of slow oscillations in the ictal state began from the temporal lobe and then spread through the whole hippocampal network via two different pathways, which might be associated with the underlying propagation of epileptiform discharges in the hippocampal network. Overall, we provide a functional description of the emergence of VFRs in the hippocampal network during SE, and we also establish that VFRs may be the physiological representation of the pathological alterations in hippocampal network activity during SE in TLE.

scholarly journals The Oscillatory Basis of Working Memory Function and Dysfunction in Epilepsy

2021 ◽  
Vol 14 ◽  
Author(s):  
Olivia N. Arski ◽  
Julia M. Young ◽  
Mary-Lou Smith ◽  
George M. Ibrahim
Keyword(s):  
Working Memory ◽  
High Frequency ◽  
Large Scale ◽  
Memory Function ◽  
Epileptic Activity ◽  
Functional Roles ◽  
High Frequency Oscillations ◽  
Epileptiform Discharges ◽  
Interictal Epileptiform Discharges

Working memory (WM) deficits are pervasive co-morbidities of epilepsy. Although the pathophysiological mechanisms underpinning these impairments remain elusive, it is thought that WM depends on oscillatory interactions within and between nodes of large-scale functional networks. These include the hippocampus and default mode network as well as the prefrontal cortex and frontoparietal central executive network. Here, we review the functional roles of neural oscillations in subserving WM and the putative mechanisms by which epilepsy disrupts normative activity, leading to aberrant oscillatory signatures. We highlight the particular role of interictal epileptic activity, including interictal epileptiform discharges and high frequency oscillations (HFOs) in WM deficits. We also discuss the translational opportunities presented by greater understanding of the oscillatory basis of WM function and dysfunction in epilepsy, including potential targets for neuromodulation.

scholarly journals Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61Substrates Involved in Hippocampal Synaptic Plasticity

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Sung-Soo Jang ◽  
Sara E. Royston ◽  
Gunhee Lee ◽  
Shuwei Wang ◽  
Hee Jung Chung
Keyword(s):  
Synaptic Plasticity ◽  
Neurodegenerative Disorder ◽  
Tyrosine Phosphatase ◽  
Amyloid Β ◽  
Epileptic Seizures ◽  
Network Activity ◽  
Extracellular Signal ◽  
Nmdar Subunit ◽  
Hippocampal Network ◽  
Electroconvulsive Seizures

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. Pathologic accumulation of soluble amyloid-β(Aβ) oligomers impairs synaptic plasticity and causes epileptic seizures, both of which contribute to cognitive dysfunction in AD. However, whether seizures could regulate Aβ-induced synaptic weakening remains unclear. Here we show that a single episode of electroconvulsive seizures (ECS) increased protein expression of membrane-associated STriatal-Enriched protein tyrosine Phosphatase (STEP61) and decreased tyrosine-phosphorylation of its substrates N-methyl D-aspartate receptor (NMDAR) subunit GluN2B and extracellular signal regulated kinase 1/2 (ERK1/2) in the rat hippocampus at 2 days following a single ECS. Interestingly, a significant decrease in ERK1/2 expression and an increase in APP and Aβlevels were observed at 3-4 days following a single ECS when STEP61level returned to the baseline. Given that pathologic levels of Aβincrease STEP61activity and STEP61-mediated dephosphorylation of GluN2B and ERK1/2 leads to NMDAR internalization and ERK1/2 inactivation, we propose that upregulation of STEP61and downregulation of GluN2B and ERK1/2 phosphorylation mediate compensatory weakening of synaptic strength in response to acute enhancement of hippocampal network activity, whereas delayed decrease in ERK1/2 expression and increase in APP and Aβexpression may contribute to the maintenance of this synaptic weakening.

scholarly journals Spontaneous EEG-Functional MRI in Mesial Temporal Lobe Epilepsy: Implications for the Neural Correlates of Consciousness

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Zheng Wang ◽  
Loretta Norton ◽  
R. Matthew Hutchison ◽  
John R. Ives ◽  
Seyed M. Mirsattari
Keyword(s):  
Temporal Lobe ◽  
Animal Studies ◽  
Brain Activity ◽  
Epileptic Seizures ◽  
Mesial Temporal Lobe Epilepsy ◽  
Unified Framework ◽  
Epileptiform Discharges ◽  
Interictal Epileptiform Discharges ◽  
Mesial Temporal Lobe ◽  
Hemodynamic Processes

The combination of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) has been shown to have great potential for providing a greater understanding of normal and diseased states in both human and animal studies. Simultaneous EEG-fMRI is particularly well suited for the study of epilepsy in that it may reveal the neurobiology of ictal and interictal epileptiform discharges and noninvasively localize epileptogenic foci. Spontaneous, coherent fluctuations of neuronal activity and the coupled hemodynamic responses have also been shown to provide diagnostic markers of disease, extending our understanding of intrinsically structured ongoing brain activity. Following a short summary of the hardware and software development of simultaneous EEG-fMRI, this paper reviews a unified framework of integrating neuronal and hemodynamic processes during epileptic seizures and discusses the role and impact of spontaneous activity in the mesial temporal lobe epilepsies with particular emphasis on the neural and physiological correlates of consciousness.

scholarly journals Circulating P2X7 Receptor Signaling Components as Diagnostic Biomarkers for Temporal Lobe Epilepsy

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2444
Author(s):  
Giorgia Conte ◽  
Aida Menéndez-Méndez ◽  
Sebastian Bauer ◽  
Hany El-Naggar ◽  
Mariana Alves ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Blood Cell ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Plasma Levels ◽  
P2x7 Receptor ◽  
Inflammatory Marker ◽  
Epileptic Seizures ◽  
Egfp Reporter ◽  
Signaling Components

Circulating molecules have potential as biomarkers to support the diagnosis of epilepsy and to assist with differential diagnosis, for example, in conditions resembling epilepsy, such as in psychogenic non-epileptic seizures (PNES). The P2X7 receptor (P2X7R) is an important regulator of inflammation and mounting evidence supports its activation in the brain during epilepsy. Whether the P2X7R or P2X7R-dependent signaling molecules can be used as biomarkers of epilepsy has not been reported. P2X7R levels were analyzed by quantitative ELISA using plasma samples from controls and patients with temporal lobe epilepsy (TLE) or PNES. Moreover, blood cell P2X7R expression and P2X7R-dependent cytokine signature was measured following status epilepticus in P2X7R-EGFP reporter, wildtype, and P2X7R-knockout mice. P2X7R plasma levels were higher in TLE patients when compared with controls and patients with PNES. Plasma levels of the broad inflammatory marker protein C-Reactive protein (CRP) were similar between the three groups. Using P2X7R-EGFP reporter mice, we identified monocytes as the main blood cell type expressing P2X7R after experimentally evoked seizures. Finally, cytokine array analysis in P2X7R-deficient mice identified KC/GRO as a potential P2X7R-dependent plasma biomarker following status epilepticus and during epilepsy. Our data suggest that P2X7R signaling components may be a promising subclass of circulating biomarkers to support the diagnosis of epilepsy.

scholarly journals Characterizing Hippocampal Oscillatory Signatures Underlying Seizures in Temporal Lobe Epilepsy

2021 ◽  
Vol 15 ◽  
Author(s):  
Thato Mary Mokhothu ◽  
Kazumasa Zen Tanaka
Keyword(s):  
Animal Models ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
High Frequency ◽  
Epileptic Seizures ◽  
Salient Feature ◽  
Future Studies ◽  
High Frequency Oscillations ◽  
Arduous Task ◽  
Brain Hyperexcitability

Temporal Lobe Epilepsy (TLE) is a neurological condition characterized by focal brain hyperexcitability, resulting in abnormal neuronal discharge and uncontrollable seizures. The hippocampus, with its inherently highly synchronized firing patterns and relatively high excitability, is prone to epileptic seizures, and it is usually the focus of TLE. Researchers have identified hippocampal high-frequency oscillations (HFOs) as a salient feature in people with TLE and animal models of this disease, arising before or at the onset of the epileptic event. To a certain extent, these pathological HFOs have served as a marker and a potential target for seizure attenuation using electrical or optogenetic interventions. However, many questions remain about whether we can reliably distinguish pathological from non-pathological HFOs and whether they can tell us about the development of the disease. While this would be an arduous task to perform in humans, animal models of TLE provide an excellent opportunity to study the characteristics of HFOs in predicting how epilepsy evolves. This minireview will (1) summarize what we know about the oscillatory disruption in TLE, (2) summarize knowledge about oscillatory changes in the latent period and their role in predicting seizures, and (3) propose future studies essential to uncovering potential treatments based on early detection of pathological HFOs.

Analysis of the acute neuroinflammatory response and endogenous markers in the amygdala of animals submitted to status epilepticus by intrahippocampal pilocarpine application

2021 ◽  
Vol 2 (6) ◽  
Author(s):  
Vinicius Lisboa Da Rocha ◽  
Amanda Pinato Alves da Costa ◽  
Amanda Feltrin Lisboa ◽  
Enzo Da Silva Salmazo ◽  
Emanoel de Oliveira Araújo ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Experimental Model ◽  
Temporal Lobe ◽  
Inflammatory Process ◽  
Epileptic Seizures ◽  
Immunohistochemical Analysis ◽  
Sterile Saline ◽  
Male Wistar Rats ◽  
The Right

Introduction: Experimental evidence and clinical evidence indicate that the inflammatory process is a crucial mechanism in the pathophysiology of epileptic seizures and temporal lobe epilepsy. The amygdala when involved in an atypical processing is associated with multiple moods such as depression and anxiety disorder and psychiatric disorders such as schizophrenia. Objective: This study investigated the acute inflammatory process and modulation of the endogenous proteins’ galectins and AnxA1 in the amygdala of animals submitted to an experimental model of temporal lobe epilepsy. Methods: The experimental procedures were approved by the Ethics Committee on the Use of Animals at UNIFESP (CEUA nº2958050814). The experiments performed in this study used data and materials that were obtained from the project “Neuroprotective and anti-inflammatory role of the mimetic peptide ac2-26 of the annexin a1 protein in intrahippocampal pilocarpine-induced status epilepticus” conducted by the advisor. The experimental model used male Wistar rats that were divided into 3 experimental groups (NAIVE; SHAM, Status Epilepticus or SE - n = 5 animals/group). Once acclimated, the animals in the SHAM and SE groups underwent stereotaxic surgery for implantation of the intracerebral cannula in the right hippocampus. The SHAM animals received sterile saline in all procedures and the NAIVE group only manipulated. The animals were monitored throughout the period and after 24 hours of experiment all animals were euthanized by overdose of thiopental to remove the brain and performed histological and immunohistochemical analysis. Results and Conclusion: Initial results demonstrate that SE and the acute inflammatory process cause damage to the amygdala, and there is also modulation of inflammatory markers in this structure. However, further studies are needed to better understand the mechanism of action in neuroinflammation in status epilepticus.

scholarly journals Hippocampal adult-born granule cells drive network activity in a mouse model of chronic temporal lobe epilepsy

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
F. T. Sparks ◽  
Z. Liao ◽  
W. Li ◽  
A. Grosmark ◽  
I. Soltesz ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Granule Cells ◽  
Topic Model ◽  
Network Activity ◽  
Relative Contribution ◽  
Epileptiform Discharges ◽  
Interictal Epileptiform Discharges ◽  
Cell Type Specific ◽  
Specific Contribution

AbstractTemporal lobe epilepsy (TLE) is characterized by recurrent seizures driven by synchronous neuronal activity. The reorganization of the dentate gyrus (DG) in TLE may create pathological conduction pathways for synchronous discharges in the temporal lobe, though critical microcircuit-level detail is missing from this pathophysiological intuition. In particular, the relative contribution of adult-born (abGC) and mature (mGC) granule cells to epileptiform network events remains unknown. We assess dynamics of abGCs and mGCs during interictal epileptiform discharges (IEDs) in mice with TLE as well as sharp-wave ripples (SPW-Rs) in healthy mice, and find that abGCs and mGCs are desynchronized and differentially recruited by IEDs compared to SPW-Rs. We introduce a neural topic model to explain these observations, and find that epileptic DG networks organize into disjoint, cell-type specific pathological ensembles in which abGCs play an outsized role. Our results characterize identified GC subpopulation dynamics in TLE, and reveal a specific contribution of abGCs to IEDs.

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