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| Research article summary (published 30 Jan 2002): |
Novel expression of AMPA-receptor subunit GluR1 on mossy cells and CA3 pyramidal neurons in the human epileptogenic hippocampus.
Full Abstract
Previous immunocytochemical investigations performed in our laboratory on the human hippocampus surgically resected for the treatment of mesial temporal lobe epilepsy (MTLE) have demonstrated an increased expression of the AMPA-receptor subunit GluR1 on neurons in the hilus and area CA3. Light microscopically, many of these neurons exhibited peculiar filamentous extensions and grape-like excrescences that protruded from their somata and proximal dendrites, suggesting that these neurons may be mossy cells and CA3 pyramidal neurons, respectively. The present electron microscopic study was carried out to further characterize these cells. The filamentous extensions were identified as dendrites from which spines often protruded, and the grape-like excrescences represented clusters of closely associated dendrites and spines. A variety of synapses were formed by the GluR1-positive profiles. These arrangements ranged from simple contacts between a single unlabelled axon terminal and a single labelled postsynaptic element, to complex contacts involving multiple unlabelled axon terminals and labelled postsynaptic elements. Many of the axon terminals involved in these arrangements were mossy fibre boutons. Thus, a large proportion of the GluR1-positive neurons were identified as hilar mossy cells and CA3 pyramidal neurons, cells hitherto thought to be absent or greatly reduced in the MTLE hippocampus. Taken together, these data suggest the presence of a highly efficient excitatory circuit involving AMPA receptors, mossy cells and CA3 pyramidal neurons in the sclerotic hippocampus. Such a circuit could be critically involved in the genesis and maintenance of temporal lobe epilepsy.
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Author information
Author/s: Eid, Tore (T); Kovacs, Ilona (I); Spencer, Dennis D (DD); de Lanerolle, Nihal C (NC);
Affiliation: Department of Neurosurgery, Yale University School of Medicine, 333 Cedar Street, PO Box 208082, New Haven, CT 06520-8082, USA. tore.eid(-atsign-)yale.edu
Grants: P01 NS39092-02 (Agency:United States NINDS)
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
Journal: The European journal of neuroscience (Eur J Neurosci), published in France. (Language: eng)
Reference: 2002-Feb; vol 15 (issue 3) : pp 517-27
Dates: Created 2002/03/05; Completed 2002/05/07; Revised 2007/11/14;
PMID: 11876779, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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