scholarly journals Manganese-enhanced magnetic resonance imaging in the acute phase of the pilocarpine-induced model of epilepsy

2012 ◽  
Vol 10 (2) ◽  
pp. 247-252 ◽  
Author(s):  
Jackeline Moraes Malheiros ◽  
Beatriz Monteiro Longo ◽  
Alberto Tannús ◽  
Luciene Covolan

Magnetic resonance images are useful in the study of experimental models of temporal lobe epilepsy. The manganese-enhanced MRI (MEMRI) technique is of interest since it combines the effects caused by manganese on the increased contrast in activated cell populations, when competing with calcium in synaptic transmission. Thus, the purpose of this study was to investigate the temporal evolution of the contrast related to manganese in the acute phase of temporal lobe epilepsy induced by systemic pilocarpine and compare it to the expression of the c-Fos protein. During this phase, the intensity of the MEMRI signal was analyzed at three different time points (5, 15 or 30 minutes) after the onset of status epilepticus (SE). The group that was maintained in status epilepticus for 30 minutes showed a decrease in intensity of the signal in CA1 and the dentate gyrus (DG). There were no differences between the control group and the other groups treated with pilocarpine. The expression of the protein, c-Fos, in the same animals showed that even in the short-duration status epilepticus (5 minutes), there was already maximal cellular activation in subregions of the hippocampus (DG, CA1 and CA3). Under the experimental conditions tested, our data suggest that the MEMRI signal was not sensitive for the identification of detectable variations of cell activation in the acute phase of the pilocarpine model. Our findings are not consistent with the idea that manganese contrast reflects primarily alterations in cellular activity during SE when other signal-modifying elements can act.

1991 ◽  
Vol 74 (4) ◽  
pp. 660-664 ◽  
Author(s):  
Howard M. Eisenberg ◽  
Andrew C. Papanicolaou ◽  
Stephen B. Baumann ◽  
Robert L. Rogers ◽  
Linda M. Brown

✓ The reliability of localization of interictal spike sources using magnetoencephalography (MEG) was examined by repeated measurements in a patient with temporal lobe epilepsy. During two preoperative recording sessions, the estimated sources, projected onto magnetic resonance images of the patient's brain, were found to lie less than 1 cm apart within the area subsequently resected. The MEG localization was in close agreement with intraoperative cortical recordings.


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0246068
Author(s):  
Daniel Ramandi ◽  
Mahmoud Elahdadi Salmani ◽  
Ali Moghimi ◽  
Taghi Lashkarbolouki ◽  
Masoud Fereidoni

It is known that hippocampal epileptogenesis is accompanied by hyperexcitability, glutamate-related neuronal dysfunctions and consequently cognitive deficits. However, the neuroprotective role of astrocytic glutamate uptake through the Glutamate Transporter-1 (GLT-1) remains to be unknown in these processes. Therefore, to assess the effect of glutamate uptake, pharmacological upregulation of GLT-1 using ceftriaxone administration (200 mg/kg/day, i.p, 5 days) was utilized in Li-PIL animal models of temporal lobe epilepsy (TLE). Glutamate concentration and glutamine synthetase activity were analyzed using biochemical assays. In addition, GLT-1 gene expression was assessed by RT-qPCR. Finally, cognitive function was studied using Morris water maze (MWM) test and novel object recognition task (NORT). Our results demonstrated that the acute phase of epileptogenesis (first 72 hours after Status Epilepticus) was accompanied by an increase in the hippocampal glutamate and downregulation of GLT-1 mRNA expression compared to controls. Ceftriaxone administration in epileptic animals led to a reduction of glutamate along with elevation of the level of glutamine synthetase activity and GLT-1 expression in the acute phase. In the chronic phase of epileptogenesis (4 weeks after Status Epilepticus), glutamate levels and GLT-1 expression were decreased compared to controls. Ceftriaxone treatment increased the levels of GLT-1 expression. Furthermore, impaired learning and memory ability in the chronic phase of epileptogenesis was rescued by Ceftriaxone administration. This study shows that astrocytic glutamate uptake can profoundly impact the processes of hippocampal epileptogenesis through the reduction of glutamate-induced excitotoxicity and consequently rescuing of cognitive deficits caused by epilepsy.


2016 ◽  
Vol 43 (1) ◽  
pp. 538-553 ◽  
Author(s):  
Mohammad-Parsa Hosseini ◽  
Mohammad-Reza Nazem-Zadeh ◽  
Dario Pompili ◽  
Kourosh Jafari-Khouzani ◽  
Kost Elisevich ◽  
...  

2020 ◽  
Author(s):  
Giorgia Conte ◽  
Alberto Parras ◽  
Mariana Alves ◽  
Ivana Ollà ◽  
Laura de Diego-Garcia ◽  
...  

AbstractObjectivePharmacoresistance and the lack of disease-modifying actions of current anti-seizure drugs persist as major challenges in the treatment of epilepsy. Experimental models of chemoconvulsant-induced status epilepticus remain the models of choice to discover potential anti-epileptogenic drugs but doubts remain as to the extent to which they model human pathophysiology. The aim of the present study was to compare the molecular landscape of the intraamygdala kainic acid model of status epilepticus in mice with findings in resected brain tissue from patients with drug-resistant temporal lobe epilepsy (TLE).MethodsStatus epilepticus was induced via intraamygdala microinjection of kainic acid in C57BL/6 mice and gene expression analysed via microarrays in hippocampal tissue at acute and chronic time-points. Results were compared to reference datasets in the intraperitoneal pilocarpine and intrahippocampal kainic acid model and to human resected brain tissue (hippocampus and cortex) from patients with drug-resistant TLE.ResultsIntraamygdala kainic acid injection in mice triggered extensive dysregulation of gene expression which was ∼3-fold greater shortly after status epilepticus (2729 genes) when compared to epilepsy (412). Comparison to samples of patients with TLE revealed a particular high correlation of gene dysregulation during established epilepsy. Pathway analysis found suppression of calcium signalling to be highly conserved across different models of epilepsy and patients. CREB was predicted as one of the main up-stream transcription factors regulating gene expression during acute and chronic phases and inhibition of CREB reduced seizure severity in the intraamygdala kainic acid model.SignificanceOur findings suggest the intraamygdala kainic acid model faithfully replicates key molecular features of human drug-resistant temporal lobe epilepsy and provides potential rationale target approaches for disease-modification through new insights into the unique and shared gene expression landscape in experimental epilepsy.Key point boxMore genes show expression changes shortly following intraamygdala kainic acid-induced status epilepticus when compared to established epilepsy.The intraamygdala kainic acid mouse model mimics closely the gene expression landscape in the brain of patients with temporal lobe epilepsy.Supressed calcium signalling in the brain as common feature across experimental models of epilepsy and patients with temporal lobe epilepsy.CREB is a major up-stream transcription factor during early changes following status epilepticus and once epilepsy is established.


2021 ◽  
Vol 22 (8) ◽  
pp. 3860
Author(s):  
Elisa Ren ◽  
Giulia Curia

Temporal lobe epilepsy (TLE) is one of the most common types of focal epilepsy, characterized by recurrent spontaneous seizures originating in the temporal lobe(s), with mesial TLE (mTLE) as the worst form of TLE, often associated with hippocampal sclerosis. Abnormal epileptiform discharges are the result, among others, of altered cell-to-cell communication in both chemical and electrical transmissions. Current knowledge about the neurobiology of TLE in human patients emerges from pathological studies of biopsy specimens isolated from the epileptogenic zone or, in a few more recent investigations, from living subjects using positron emission tomography (PET). To overcome limitations related to the use of human tissue, animal models are of great help as they allow the selection of homogeneous samples still presenting a more various scenario of the epileptic syndrome, the presence of a comparable control group, and the availability of a greater amount of tissue for in vitro/ex vivo investigations. This review provides an overview of the structural and functional alterations of synaptic connections in the brain of TLE/mTLE patients and animal models.


2013 ◽  
Vol 27 (1) ◽  
pp. 174-187 ◽  
Author(s):  
Jana Tchekalarova ◽  
Zlatina Petkova ◽  
Daniela Pechlivanova ◽  
Slavianka Moyanova ◽  
Lidia Kortenska ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document