Possible mechanisms inducing granule cell dispersion in humans with temporal lobe epilepsy

Lurton, Dominique; Sundström, Lars; Brana, Corinne; Bloch, Bertrand; Rougier, Alain

doi:10.1016/s0920-1211(96)01002-9

Cited by 48 publications

(40 citation statements)

References 27 publications

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“…However, the role of these receptors in GCD, one of the most important structural changes observed in the hippocampus of 50% of MTLE patients, has not been studied yet (1,5,6).…”

Section: Involvement Of Glutamatergic Neurotransmissionmentioning

confidence: 99%

“…Sprouting of mossy fibers into the inner molecular layer and granule cell dispersion (GCD) of the dentate gyrus also are commonly associated with HS in MTLE patients (4)(5)(6)(7)(8). GCD is characterized by an enlargement of stratum granulosum, a loss of the close apposition between granule cell soma, and the presence of granule cells scattered in the molecular layer with an elongated bipolar change of cell bodies (5).…”

mentioning

confidence: 99%

“…Previous articles have reported that the presence of GCD was significantly associated with epileptic activities arising during the first 4 years of life in humans (6). It could also be induced by seizure-linked structural plasticity occurring during the specific early sensitive period of brain maturation (5,6). However, recent studies failed to show a significant correlation between early seizure onset and the extent of GCD (1,9,12,13).…”

mentioning

confidence: 99%

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Glutamate Receptor Antagonists and Benzodiazepine Inhibit the Progression of Granule Cell Dispersion in a Mouse Model of Mesial Temporal Lobe Epilepsy

et al. 2005

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Summary:Purpose: Unilateral intrahippocampal injection of kainic acid (KA) in adult mice induces the progressive dispersion of dentate granule cells, one of the characteristic pathologic changes of mesial temporal lobe epilepsy. However, little is known about the mechanisms that trigger this dispersion. In this study, the possible involvement of glutamatergic and γ -aminobutyric acid (GABA)ergic neurotransmissions in the development of granule cell dispersion (GCD) was examined in this model.Methods: Antagonists of N-methyl-D-aspartate (NMDA) receptor (MK-801) and non-NMDA receptor (GYKI52466), and an agonist of benzodiazepine-GABA A receptor (midazolam) were injected before and after KA in various ways, and the morphologic changes of the hippocampus, especially GCD, were examined.Results: MK-801 (5 mg/kg, i.p.) did not reduce GCD when injected 2 h before KA injection but inhibited GCD almost completely for ≤14 days, when injected 4 h after KA. However, mild to moderate dispersion was observed at 28 days, indicating that MK-801 may delay the progression of GCD. Similarly, daily treatment with MK-801 (2 × 1 mg/kg i.p./day) for the first 26 days after KA significantly reduced GCD. In contrast, GYKI52466 (30 mg/kg, s.c.) was effective only when it was injected before KA. A significant reduction of GCD was also observed after continuous administration of midazolam (10 mg/kg/h) after KA.Conclusions: These data show that GCD in this mouse model is triggered by either the stimulation of the NMDA receptor or reduction of GABA A -mediated inhibition after intrahippocampal injection of KA. It is suggested that the increased excitation or the reduced inhibition or both could be one of the factors triggering or maintaining or both the process of GCD.

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“…However, the role of these receptors in GCD, one of the most important structural changes observed in the hippocampus of 50% of MTLE patients, has not been studied yet (1,5,6).…”

Section: Involvement Of Glutamatergic Neurotransmissionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Glutamate Receptor Antagonists and Benzodiazepine Inhibit the Progression of Granule Cell Dispersion in a Mouse Model of Mesial Temporal Lobe Epilepsy

et al. 2005

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“…Many pathological conditions, such as epilepsy (Houser, 1990;Lurton et al, 1997;Haas et al, 2002), lissencephaly (Sato et al, 2001;Ross et al, 2001), Down's syndrome (Raz et al, 1995), and psychiatric disorders (Benes and Berretta, 2001;Connor et al, 2004) are associated with histological abnormalities in the hippocampus, and the abnormalities are likely to be related to a disruption of neuronal migration during development. Thus, knowledge of neuronal migration during hippocampal histogenesis is necessary to be able to analyze the pathogenesis of the above conditions.…”

mentioning

confidence: 99%

Neuronal generation, migration, and differentiation in the mouse hippocampal primoridium as revealed by enhanced green fluorescent protein gene transfer by means of in utero electroporation

Nakahira

Yuasa

2005

J of Comparative Neurology

105

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Neuronal migration defects in the hippocampus during development are thought to be involved in various mental disorders. Studies of neural cell migration in the developing cerebrum have focused mainly on the neocortex, but those that have been performed on the developing hippocampal formation have not been adequately carried out. In the present study, the morphological differentiation of immature neurons that form the laminar structure of the hippocampus was investigated by labeling ventricular surface cells with the expression vector of the enhanced-green-fluorescent-protein (EGFP) gene. Vector DNA was transfected into spatially and temporally restricted neuroepithelium of the hippocampal primordium by in utero electroporation, and the morphology of EGFP-labeled migratory neurons and their interrelationships with the radial glial arrangement were observed. Pyramidal cells of Ammon's horn began to migrate radially along glial processes from a broad area of neuroepithelium on embryonic day (E)14. Large numbers of multipolar cells were found in the intermediate zone in the initial stage and stratified pyramidal cells appeared later. Dentate granule cells were labeled later than (E)16 and originated from a restricted area of neuroepithelium adjacent to the fimbria. Their initial migration was rapid and independent of radial glial fibers. Subsequent tangential migration in the subpial space and their ultimate settling into the forming dentate gyrus were closely associated with the radial glia. These findings indicate that distinct cellular mechanisms are involved in the development of the cortical layer of Ammon's horn and dentate gyrus.

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“…It has remained unclear whether the appearance of heterotopic granule cells is related to granule cell loss in the epileptic hippocampus. Granule cell dispersion has not been observed when a cell loss is minimal (Lurton et al, 1997). We also determined decreased number of neurons in the GD region in the acute-and chronic-PTZ groups.There was a significant difference between the number of GD neurons between the gropus .…”

Section: Discussionmentioning

confidence: 99%

Cellular and Molecular Mechanisms Underlying Epilepsy: An Overview with Our Findings

Yardımoğlu¹,

İlbay²,

Dalçįk³

et al. 2012

Epilepsy - Histological, Electroencephalographic and Psychological Aspects

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Possible mechanisms inducing granule cell dispersion in humans with temporal lobe epilepsy

Cited by 48 publications

References 27 publications

Glutamate Receptor Antagonists and Benzodiazepine Inhibit the Progression of Granule Cell Dispersion in a Mouse Model of Mesial Temporal Lobe Epilepsy

Glutamate Receptor Antagonists and Benzodiazepine Inhibit the Progression of Granule Cell Dispersion in a Mouse Model of Mesial Temporal Lobe Epilepsy

Neuronal generation, migration, and differentiation in the mouse hippocampal primoridium as revealed by enhanced green fluorescent protein gene transfer by means of in utero electroporation

Cellular and Molecular Mechanisms Underlying Epilepsy: An Overview with Our Findings

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