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Titolo:
Loss of hilar mossy cells in Ammon's horn sclerosis
Autore:
Blumcke, I; Suter, B; Behle, K; Kuhn, R; Schramm, J; Elger, CE; Wiestler, OD;
Indirizzi:
Univ Bonn, Med Ctr, Dept Neuropathol, D-53105 Bonn, Germany Univ Bonn Bonn Germany D-53105 , Dept Neuropathol, D-53105 Bonn, Germany Univ Bonn, Med Ctr, Dept Neurosurg, D-53105 Bonn, Germany Univ Bonn BonnGermany D-53105 tr, Dept Neurosurg, D-53105 Bonn, Germany Univ Bonn, Med Ctr, Dept Epileptol, D-53105 Bonn, Germany Univ Bonn BonnGermany D-53105 tr, Dept Epileptol, D-53105 Bonn, Germany Novartis Pharmaceut, CNS Res, Basel, Switzerland Novartis Pharmaceut Basel Switzerland ceut, CNS Res, Basel, Switzerland
Titolo Testata:
EPILEPSIA
, volume: 41, anno: 2000, supplemento:, 6
pagine: S174 - S180
SICI:
0013-9580(2000)41:<S174:LOHMCI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
TEMPORAL-LOBE EPILEPSY; CALRETININ-IMMUNOREACTIVE NEURONS; FIBER SYNAPTIC REORGANIZATION; RAT FASCIA-DENTATA; GRANULE CELLS; INTRACELLULAR-RECORDINGS; PRESURGICAL EVALUATION; POSTNATAL-DEVELOPMENT; HIPPOCAMPAL SLICES; PERFORANT PATH;
Keywords:
hippocampus; mGluR; confocal laser scanning microscopy; epilepsy; Ammon's horn sclerosis; seizures; temporal lobe epilepsy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Blumcke, I Univ Bonn, Med Ctr, Dept Neuropathol, Sigmund Freud Str 25, D-53105 Bonn, Germany Univ Bonn Sigmund Freud Str 25 Bonn Germany D-53105 n, Germany
Citazione:
I. Blumcke et al., "Loss of hilar mossy cells in Ammon's horn sclerosis", EPILEPSIA, 41, 2000, pp. S174-S180

Abstract

Purpose: Hilar mossy cells represent an important excitatory subpopulationof the hippocampal formation. Several studies have identified this cell type as particularly vulnerable to seizure activity in rat models of limbic epilepsy. Hen we have subjected hilar mossy cell loss in the hippocampus of patients with chronic temporal lobe epilepsy (TLE) to a systematic morphological and immunohistochemical analysis. Methods: Hippocampal specimens from 30 TLE patients were included; 21 patients presented with segmental neuronal cell loss [Ammon's horns clerosis (AHS)] and 8 with focal Lesions (tumors, scars, malformations) not involving the hippocampus proper. In one additional TLE patient, no histopathologicalalteration could be observed. Surgical specimens from tumor patients without epilepsy (n = 2) and nonepileptic autopsy brains(n = 8) were used as controls. Hilar mossy cells in the human hippocampus were visualized using a novel poly cloncal antiserum directed against the metabotropic glutamate receptor subtype mGluR7b or by intracellular Lucifer Yellow injection. confocal laser scanning microscopy, and three-dimensional morphological reconstruction. Results: Compared with controls, a significant loss of mGluR7 immunoreactive mossy cells was observed in patients with AHS (p < 0.05). In contrast, TLE patients with focal lesions but structurally intact hippocampus demonstrated only a discrete, nonsignificant reduction of this neuronal subpopulation, This observation was confirmed by analysis of 62 randomly injected hilar neurons from AHS patients, in which we were unable to detect neurons witha morphology like that of hilar mossy cells. Conclusion: Our present data indicate significant hilar mossy cell loss inTLE patients with AHS. In contrast, hilar mossy cells appear to be less vulnerable in patients with lesion-associated TLE. Although the significance of mGluR7 immunoreactivity in mossy cells remains to be studied, loss of this cell population is compatible with alterations in hippocampal networks and regional hyperexcitability as pathogenic mechanism of AHS and TLE.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 11:29:47