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  • 1
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Gamma aminobutyric acid ; Receptor ; Ammon's horn sclerosis ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations of gamma aminobutyric acid (GABA)-mediated neurotransmission have been implicated in the pathogenesis of epilepsies. Here we examine the distribution of the GABAA receptor in the hippocampus of 78 surgical specimens from patients with chronic pharmacoresistant focal epilepsies. The receptor was localized immunohistochemically with the monoclonal antibody bd-24 which selectively recognizes the α1 subunit of the GABAA receptor. The results were compared with the receptor distribution of 28 normal hippocampal specimens obtained at autopsy. In the great majority of the surgical specimens a loss of GABAA receptor immunoreactivity was present in CA1 (92.3  %), CA4 (78.2  %), the dentate granular cell layer (70.5  %) and the molecular layer of the dentate gyrus (65.4  %). The subiculum revealed a normal staining pattern in all but 4 cases. In no instance did we observe an increase of immunoreactivity in any region or cell population. The decrease of GABAA receptor immunoreactivity was closely related to neuronal loss in the respective specimen and to Ammon's horn sclerosis. There was no correlation between GABAA receptor loss and the patient's age at surgery, duration of seizures, age at onset of seizures and to the presence or absence of secondary generalized tonic clonic seizures. The data suggest that the observed loss of GABAA receptor immunoreactivity is a secondary phenomenon rather than an event that is relevant for the pathogenesis of epileptic seizures.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Immunohistochmistry ; Receptor ; Neurotransmitter ; Tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Oligodendrogliomas and dysembryoplastic neuroepithelial tumors (DNT) are frequently associated with epilepsies and share the presence of oligodendroglia-like cells with small round nuclei and optically empty perinuclear halos. The two entities may be difficult to discriminate in small surgical specimens and the origin and differentiation of the oligodendroglia-like cells has been controversial. To better characterize and distinguish the two entities we examined 25 oligodendrogliomas and 16 DNT immunohistochemically for the presence of the proliferation–associated Ki-67 antigen and the following neural antigens: the α1 subunit of the GABAA receptor (GABAR), N-methyl-d-aspartate receptor subunit 1 (NR1), glutamate decarboxylase, neuronal nuclei antigen (NeuN), the embryonal form of the neural cell adhesion molecule (E-NCAM), synaptophysin, neurofilament protein (NFP), and glial fibrillary acidic protein (GFAP). Labeling indices for the Ki-67 antigens were generally less than 1% in both entities. In oligodendrogliomas, more than 50% of the tumors contained NR1- or E-NCAM-positive oligodendroglia-like cells, whereas NeuN-positive tumor cells were never observed. In DNT, NeuN- and NR1-positive tumor cells were present in 44% of the cases each; E-NCAM positivity was less frequent (19%). In both entities, immunoreactivity of oligodendroglia-like cells for GABAR and glutamate decarboxylase was rare and positivity for synaptophysin and neurofilament protein was absent. Some GFAP-positive tumor cells were present in approximately 70% of the cases in both entities. Except for the striking difference in NeuN positivity, the immunohistochemical profiles of oligodendroglia-like cells in DNT and oligodendrogliomas largely overlap and the differential diagnosis continues to rest mainly on conventional histopathological features. The NR1 positivity and the recently reported generation of action potentials in oligodendroglioma cells are consistent with neuronal differentiation and may contribute to the high epileptogenic potential of oligodendrogliomas.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Epilepsy ; Gamma aminobutyric acid ; Receptor ; Ammon's horn sclerosis ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations of gamma aminobutyric acid (GABA)-mediated neurotransmission have been implicated in the pathogenesis of epilepsies. Here we examine the distribution of the GABAA receptor in the hippocampus of 78 surgical specimens from patients with chronic pharmacoresistant focal epilepsies. The receptor was localized immunohistochemically with the monoclonal antibody bd-24 which selectively recognizes the α1 subunit of the GABAA receptor. The results were compared with the receptor distribution of 28 normal hippocampal specimens obtained at autopsy. In the great majority of the surgical specimens a loss of GABAA receptor immunoreactivity was present in CA1 (92.3%), CA4 (78.2%), the dentate granular cell layer (70.5%) and the molecular layer of the dentate gyrus (65.4%). The subiculum revealed a normal staining pattern in all but 4 cases. In no instance did we observe an increase of immunoreactivity in any region or cell population. The decrease of GABAA receptor immunoreactivity was closely related to neuronal loss in the respective specimen and to Ammon's horn sclerosis. There was no correlation between GABAA receptor loss and the patient's age at surgery, duration of seizures, age at onset of seizures and to the presence or absence of secondary generalized tonic clonic seizures. The data suggest that the observed loss of GABAA receptor immunoreactivity is a secondary phenomenon rather than an event that is relevant for the pathogenesis of epileptic seizures.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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