ArticleActa neuropathologica1995
Hippocampal loss of N-methyl-D-aspartate receptor subunit 1 mRNA in chronic temporal lobe epilepsy.
Article in Acta neuropathologica, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 34 citations in OpenAlex.
- Trigonelline as an anticonvulsant agent: mechanistic insights into NMDA receptor expression and oxidative stress balance.Scientific reports · 2024Article
- Knockdown and overexpression of NR1 modulates NMDA receptor function.Molecular and cellular neurosciences · 2009Article
- Glutamate NMDA receptor subunit R1 and GAD mRNA expression in human temporal lobe epilepsy.Cellular and molecular neurobiology · 2002Article
- Properties of single NMDA receptor channels in human dentate gyrus granule cells.The Journal of physiology · 1999Article
- Differential and time-dependent changes in gene expression for type II calcium/calmodulin-dependent protein kinase, 67 kDa glutamic acid decarboxylase, and glutamate receptor subunits in tetanus toxin-induced focal epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hippocampal distribution of mRNA for the N-methyl-D-aspartate (NMDA) receptor subunit 1 (NR1) was examined by non-radioactive in situ hybridization in 21 archival formalin-fixed and paraffin-embedded surgical specimens from patients with pharmacoresistant chronic epilepsy and in normal control specimens obtained at autopsy. Using the digoxigenin-labeling procedure, ribonucleotide probes were found to be significantly more sensitive than synthetic oligonucleotide probes. In normal autopsy specimens and in surgical specimens without Ammon's horn sclerosis there was intense NR1 expression in a great majority of the dentate gyrus granular cells. Many neurons in the hippocampal pyramidal cell layer also revealed a strong signal intensity. The strata oriens and moleculare of Ammon's horn and the molecular layer of the dentate gyrus contained only few labeled neurons. In the subiculum and entorhinal cortex most neurons throughout various layers were positive. In hippocampal specimens of patients with chronic epilepsy there was a loss of NR1-positive cells that was closely related to the overall neuronal loss in the respective specimen and to Ammon's horn sclerosis. These data suggest that the loss of NR1 expression is a secondary phenomenon rather than an event that is relevant for the pathogenesis of epileptic seizures.
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Registered trials
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