Evidence map›Paper›PMID 21110857›Full record

ArticleOrphanet journal of rare diseases2010

In vivo effects of antibodies from patients with anti-NMDA receptor encephalitis: further evidence of synaptic glutamatergic dysfunction.

Mario Manto, Josep Dalmau, Adrien Didelot, Véronique Rogemond, Jérôme Honnorat

Abstract read
In one paragraph

Article in Orphanet journal of rare diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

68 citing papers in PubMed.

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  20. Roles of N-Methyl-D-Aspartate Receptors (NMDARs) in Epilepsy.Frontiers in molecular neuroscience · 2021
    Review

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Mario MantoFNRS-Laboratoire de Neurologie Expérimentale, ULB, Belgium. mmanto@ulb.ac.be
Josep Dalmau
Adrien Didelot
Véronique Rogemond
Jérôme Honnorat

Funding

Paraneoplastic Disorders of CNS: Autoantigen ProfilingR01CA107192 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DALMAU, JOSEP O. · 2004 to 2007
$1.2M
Immunity to brain Ma proteins: A remote effect of cancerR56CA089054 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DALMAU, JOSEP O. · 2007 to 2007
$259k
NCI NIH HHS 2R56CA089054NCI NIH HHS R01CA107192
6 · The paper itself

Abstract

backgroundA severe encephalitis that associates with auto-antibodies to the NR1 subunit of the NMDA receptor (NMDA-R) was recently reported. Patients' antibodies cause a decrease of the density of NMDA-R and synaptic mediated currents, but the in vivo effects on the extracellular glutamate and glutamatergic transmission are unknown.

methodsWe investigated the acute metabolic effects of patients' CSF and purified IgG injected in vivo. Injections were performed in CA1 area of Ammon's horn and in premotor cortex in rats.

resultsPatient's CSF increased the concentrations of glutamate in the extracellular space. The increase was dose-dependent and was dramatic with purified IgG. Patients' CSF impaired both the NMDA- and the AMPA-mediated synaptic regulation of glutamate, and did not affect the glial transport of glutamate. Blockade of GABA-A receptors was associated with a marked elevation of extra-cellular levels of glutamate following a pretreatment with patients' CSF.

conclusionThese results support a direct role of NMDA-R antibodies upon altering glutamatergic transmission. Furthermore, we provide additional evidence in vivo that NMDA-R antibodies deregulate the glutamatergic pathways and that the encephalitis associated with these antibodies is an auto-immune synaptic disorder.

Indexed as

AnimalsAutoantibodiesAutoimmune Diseases of the Nervous SystemEncephalitisGlutamatesHumansImmunoglobulin GMaleRatsRats, WistarReceptors, N-Methyl-D-AspartateSynaptic TransmissionAutoantibodiesGlutamatesImmunoglobulin GReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21110857
PMCPMC3002330

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.