scholarly journals Reduced Astrocytic Contribution to the Turnover of Glutamate, Glutamine, and GABA Characterizes the Latent Phase in the Kainate Model of Temporal Lobe Epilepsy

2011 ◽  
Vol 31 (8) ◽  
pp. 1675-1686 ◽  
Author(s):  
Silje Alvestad ◽  
Janniche Hammer ◽  
Hong Qu ◽  
Asta Håberg ◽  
Ole Petter Ottersen ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Time Window ◽  
Hippocampal Formation ◽  
Piriform Cortex ◽  
Mesial Temporal Lobe Epilepsy ◽  
Resonance Spectroscopy ◽  
Branched Chain ◽  
Latent Phase ◽  
Potential Biomarkers

The occurrence of spontaneous seizures in mesial temporal lobe epilepsy (MTLE) is preceded by a latent phase that provides a time window for identifying and treating patients at risk. However, a reliable biomarker of epileptogenesis has not been established and the underlying processes remain unclear. Growing evidence suggests that astrocytes contribute to an imbalance between excitation and inhibition in epilepsy. Here, astrocytic and neuronal neurotransmitter metabolism was analyzed in the latent phase of the kainate model of MTLE in an attempt to identify epileptogenic processes and potential biomarkers. Fourteen days after status epilepticus, [1-13C]glucose and [1,2-13C]acetate were injected and the hippocampal formation, entorhinal/piriform cortex, and neocortex were analyzed by 1H and 13C magnetic resonance spectroscopy. The 13C enrichment in glutamate, glutamine, and γ-aminobutyric acid (GABA) from [1-13C]glucose was decreased in all areas. Decreased GABA content was specific for the hippocampal formation, together with a pronounced decrease in astrocyte-derived [1,2-13C]GABA and a decreased transfer of glutamine for the synthesis of GABA. Accumulation of branched-chain amino acids combined with decreased [4,5-13C]glutamate in hippocampal formation could signify decreased transamination via branched-chain aminotransferase in astrocytes. The results point to astrocytes as major players in the epileptogenic process, and 13C enrichment of glutamate and GABA as potential biomarkers.

scholarly journals Neurocysticercosis and microscopic hippocampal dysplasia in a patient with refractory mesial temporal lobe epilepsy

2006 ◽  
Vol 64 (2a) ◽  
pp. 309-313 ◽  
Author(s):  
Alexandre Valotta da Silva ◽  
Heloise Helena Martins ◽  
Carolina Mattos Marques ◽  
Elza Marcia Targas Yacubian ◽  
Américo Ceiki Sakamoto ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Refractory Epilepsy ◽  
Hippocampal Formation ◽  
Granular Cell ◽  
Mesial Temporal Lobe Epilepsy ◽  
Epidemiologic Studies ◽  
Neuronal Markers ◽  
Symptomatic Epilepsy ◽  
Mesial Temporal Lobe

Epidemiologic studies suggest that neurocysticercosis (NC) is the main cause of symptomatic epilepsy in developing countries. The association between NC and mesial temporal lobe epilepsy (MTLE) has been reported by several authors. Recent data have shown that the presence of NC does not influence the clinical and pathological profile in MTLE patients and suggest that not all cysticercotic lesions are inevitably epileptogenic. We describe a 50-years-old woman with partial seizures due to NC which evolve to MTLE. The patient was submitted to a corticoamygdalohippocampectomy to treat refractory epilepsy. An immunohistochemical study using neuronal markers was made on hippocampal formation. Besides the typical aspects of Ammon's horn sclerosis (AHS), the microscopic examination demonstrates cellular features of hippocampal malformation including dysmorphic neurons and focal bilamination of granular cell layer. We suggest that, in this case, a developmental disorder lowered the threshold for the NC-induced seizures and contributed to the establishment of refractory epilepsy.

scholarly journals Metabolism is Normal in Astrocytes in Chronically Epileptic Rats: A 13C NMR Study of Neuronal—Glial Interactions in a Model of Temporal Lobe Epilepsy

2005 ◽  
Vol 25 (10) ◽  
pp. 1254-1264 ◽  
Author(s):  
Torun M Melø ◽  
Astrid Nehlig ◽  
Ursula Sonnewald
Keyword(s):  
Cerebral Cortex ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Neuronal Loss ◽  
Adenosine Diphosphate ◽  
Resonance Spectroscopy ◽  
Metabolic Disturbances ◽  
Nmr Study ◽  
Pilocarpine Model

The aim of the present work was to study potential disturbances in metabolism and interactions between neurons and glia in the lithium-pilocarpine model of temporal lobe epilepsy. Rats chronically epileptic for 1 month received [1-13C]glucose, a substrate for neurons and astrocytes, and [1,2-13C]acetate, a substrate for astrocytes only. Analyses of extracts from cerebral cortex, cerebellum, and hippocampal formation (hippocampus, amygdala, entorhinal, and piriform cortices) were performed using 13C and 1H nuclear magnetic resonance spectroscopy and HPLC. In the hippocampal formation of epileptic rats, levels of glutamate, aspartate, N-acetyl aspartate, adenosine triphosphate plus adenosine diphosphate and glutathione were decreased. In all regions studied, labeling from [1,2-13C]acetate was similar in control and epileptic rats, indicating normal astrocytic metabolism. However, labeling of glutamate, GABA, aspartate, and alanine from [1-13C]glucose was decreased in all areas possibly reflecting neuronal loss. The labeling of glutamine from [1-13C]glucose was decreased in cerebral cortex and cerebellum and unchanged in hippocampal formation. In conclusion, no changes were detected in glial—neuronal interactions in the hippocampal formation while in cortex and cerebellum the flow of glutamate to astrocytes was decreased, indicating a disturbed glutamate—glutamine cycle. This is, to our knowledge, the first study showing that metabolic disturbances are confined to neurons inside the epileptic circuit.

scholarly journals Hippocampal Formation Involvement in a Language-activation Task in Patients with Mesial Temporal Lobe Epilepsy

Epilepsia ◽  
2005 ◽  
Vol 46 (11) ◽  
pp. 1754-1763 ◽  
Author(s):  
Lisa Bartha ◽  
Peter Marien ◽  
Christian Brenneis ◽  
Thomas Trieb ◽  
Christian Kremser ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Mesial Temporal Lobe Epilepsy ◽  
Mesial Temporal Lobe ◽  
Language Activation

1H magnetic resonance spectroscopy at 3 T in cryptogenic and mesial temporal lobe epilepsy

2006 ◽  
Vol 19 (5) ◽  
pp. 544-553 ◽  
Author(s):  
Franz Riederer ◽  
Michal Bittšanský ◽  
Christian Schmidt ◽  
Vladimír Mlynárik ◽  
Christoph Baumgartner ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Mesial Temporal Lobe Epilepsy ◽  
Resonance Spectroscopy ◽  
1H Magnetic Resonance Spectroscopy ◽  
Mesial Temporal Lobe

scholarly journals Brain Mitochondrial Metabolic Dysfunction and Glutamate Level Reduction in the Pilocarpine Model of Temporal Lobe Epilepsy in Mice

2013 ◽  
Vol 33 (7) ◽  
pp. 1090-1097 ◽  
Author(s):  
Olav B Smeland ◽  
Mussie G Hadera ◽  
Tanya S McDonald ◽  
Ursula Sonnewald ◽  
Karin Borges
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Tca Cycle ◽  
Gas Chromatography Mass Spectrometry ◽  
Resonance Spectroscopy ◽  
Metabolic Dysfunction ◽  
Metabolic Characteristics ◽  
Pilocarpine Model

Although certain metabolic characteristics such as interictal glucose hypometabolism are well established for temporal lobe epilepsy (TLE), its pathogenesis still remains unclear. Here, we performed a comprehensive study of brain metabolism in a mouse model of TLE, induced by pilocarpine-status epilepticus (SE). To investigate glucose metabolism, we injected mice 3.5-4 weeks after SE with [1,2- 13 C]glucose before microwave fixation of the head. Using 1 H and 13 C nuclear magnetic resonance spectroscopy, gas chromatography—mass spectrometry and high-pressure liquid chromatography, we quantified metabolites and 13 C labeling in extracts of cortex and hippocampal formation (HF). Hippocampal levels of glutamate, glutathione and alanine were decreased in pilocarpine-SE mice compared with controls. Moreover, the contents of N-acetyl aspartate, succinate and reduced nicotinamide adenine dinucleotide (phosphate) NAD(P)H were decreased in HF indicating impairment of mitochondrial function. In addition, the reduction in 13 C enrichment of hippocampal citrate and malate suggests decreased tricarboxylic acid (TCA) cycle turnover in this region. In cortex, we found reduced 13 C labeling of glutamate, glutamine and aspartate via the pyruvate carboxylation and pyruvate dehydrogenation pathways, suggesting slower turnover of these amino acids and/or the TCA cycle. In conclusion, mitochondrial metabolic dysfunction and altered amino-acid metabolism is found in both cortex and HF in this epilepsy model.

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