Structural changes in astrocytes induced by seizures in a model of temporal lobe epilepsy

Castiglioni, Alejandro; Peterson, Steven L.; Sanabria, E. L.; Tiffany‐Castiglioni, Evelyn

doi:10.1002/jnr.490260310

Cited by 26 publications

(13 citation statements)

References 14 publications

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“…Although the morphologic changes were significantly different from control animals, they were less pronounced than in the cortex of ferrous chloride-injected mice. The severity of reactive changes of astrocytes in kainateinjected mice is consistent with the notion that the seizure foci in kainate-injected animals reside in the CA3 hippocampal region (Castiglioni et al, 1990;Ben-Ari and Cossart, 2000).…”

Section: Loss Of Domain Organization In Other Epileptic Modelssupporting

confidence: 85%

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Loss of Astrocytic Domain Organization in the Epileptic Brain

et al. 2008

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Gliosis is a pathological hallmark of posttraumatic epileptic foci, but little is known about these reactive astrocytes beyond their high glial fibrillary acidic protein (GFAP) expression. Using diolistic labeling, we show that cortical astrocytes lost their nonoverlapping domain organization in three mouse models of epilepsy: posttraumatic injury, genetic susceptibility, and systemic kainate exposure. Neighboring astrocytes in epileptic mice showed a 10-fold increase in overlap of processes. Concurrently, spine density was increased on dendrites of excitatory neurons. Suppression of seizures by the common antiepileptic, valproate, reduced the overlap of astrocytic processes. Astrocytic domain organization was also preserved in APP transgenic mice expressing a mutant variant of human amyloid precursor protein despite a marked upregulation of GFAP. Our data suggest that loss of astrocytic domains was not universally associated with gliosis, but restricted to seizure pathologies. Reorganization of astrocytes may, in concert with dendritic sprouting and new synapse formation, form the structural basis for recurrent excitation in the epileptic brain.

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Section: Loss Of Domain Organization In Other Epileptic Modelssupporting

confidence: 85%

“…8). Reactive changes of astrocytes in the opposite hemisphere were probably caused by projection of seizure discharge to this area (Castiglioni et al, 1990).…”

Section: Reactive Astrocytes In An Experimental Model Of Posttraumatimentioning

confidence: 97%

Loss of Astrocytic Domain Organization in the Epileptic Brain

et al. 2008

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“…Hippocampal neuronal loss can be induced in animals by seizure activity or subconvulsive electrical stimulation in the amygdala, hippocampus and other structures [22][23][24], even in the absence of hypoxia [25][26][27][28]. This suggests that excitotoxicity is an important mechanism of the neuronal damage in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Sclerosis: Development in Adult Life

1999

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Hippocampal sclerosis (HS) is the most common pathological lesion underyling intractable temporal lobe epilepsy. It is not known whether HS exists before the onset of epilepsy or whether it is caused by seizures. Its has been proposed that childhood seizures cause HS. Optimized magnetic resonance imaging (MRI), hippocampal volumes and T₂ signal quantitation were performed 2 weeks and 8 months following at tonic-clonic seizure in a 23-year-old man. MRI 14 days after the seizure showed symmetrical hippocampal volumes (ratio R/L = 1.03) with intact internal architecture bilaterally but marked signal change in the right hippocampus (T₂ right = 121, T₂ left = 103, normal ≤108 ms). Eight months later this hippocampus showed severe atrophy with a volume ratio of 0.65 and T₂ values of 117 (right) and 109 ms (left). High-resolution imaging showed that volume loss occurred mainly in the CA1 region which showed high signal in the initial study. Characteristic MRI features of HS can develop in adults and HS cannot always be assumed to have its origins in childhood. Hypoxia in the context of seizures may be an important component in hippocampal damage. HS may be a preventable lesion and MRI signal change seen in the neuronal layers of the hippocampus may be an indication for neuroprotection.

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“…Studies on animal models of epilepsy show that gliosis is present in regions exhibiting epileptiform activity because of neuronal injury as well as seizure activity (Castiglioni et al, 1990;Eddleston and Mucke, 1993;Khurgel and Ivy, 1996). In Li-pilotreated rats, changes in astrocytes were mainly characterized by hypertrophy of cell bodies and processes near the lesions rather than an increase in astrocyte number (Roch et al, 2002).…”

Section: Tricarboxylic Acid Cycle Derived Metabolites In the Hippocammentioning

confidence: 99%

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

Melø

Nehlig

Sonnewald

2005

J Cereb Blood Flow Metab

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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 [1-13 C]glucose, a substrate for neurons and astrocytes, and [1,2-13 C]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 13 C and 1 H 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 [1,2-13 C]acetate was similar in control and epileptic rats, indicating normal astrocytic metabolism. However, labeling of glutamate, GABA, aspartate, and alanine from [1-13 C]glucose was decreased in all areas possibly reflecting neuronal loss. The labeling of glutamine from [1-13 C]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.

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Structural changes in astrocytes induced by seizures in a model of temporal lobe epilepsy

Cited by 26 publications

References 14 publications

Loss of Astrocytic Domain Organization in the Epileptic Brain

Loss of Astrocytic Domain Organization in the Epileptic Brain

Hippocampal Sclerosis: Development in Adult Life

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

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Structural changes in astrocytes induced by seizures in a model of temporal lobe epilepsy

Cited by 26 publications

References 14 publications

Loss of Astrocytic Domain Organization in the Epileptic Brain

Loss of Astrocytic Domain Organization in the Epileptic Brain

Hippocampal Sclerosis: Development in Adult Life

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

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