Research article summary (published 2 Apr 2006):

Increase in tyrosine phosphorylation of the NMDA receptor following the induction of status epilepticus.

Full Abstract

The administration of lithium followed by pilocarpine induces status epilepticus (SE) that produces neurodegeneration and the subsequent development of spontaneous recurrent seizures. We have reported that tyrosine phosphorylation of the NMDA receptor is elevated over controls for several hours following 60 min of SE. In the current study, we assessed the temporal relationship between tyrosine phosphorylation of the NMDA receptor and the onset of SE. SE was induced using the Li/pilocarine model and phosphorylation of the NMDA receptor subunits NR2A and NR2B determined. Tyrosine phosphorylation of the NMDAR remained unchanged prior to the onset of SE and increased gradually thereafter. The onset of SE was accompanied by activation of Src-family tyrosine kinases and Pyk2 in the post-synaptic density, consistent with a role for these enzymes in SE-induced tyrosine phosphorylation. The results indicate that tyrosine phosphorylation of the NMDAR closely parallels the activation of Src-family kinases and follows, rather than precedes, the onset of SE.

Author information

Author/s: Huo, Jeanne Zhen (JZ); Dykstra, Crystal M (CM); Gurd, James W (JW);

Affiliation: Centre for the Neurobiology of Stress, Department of Life Sciences, University of Toronto at Scarborough, Toronto, Ontario, Canada M1C 1A4.

Journal and publication information

Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

Journal: Neuroscience letters (Neurosci Lett), published in Ireland. (Language: eng)

Reference: 2006-Jul; vol 401 (issue 3) : pp 266-70

Dates: Created 2006/05/24; Completed 2006/09/14; Revised 2006/11/15;

PMID: 16600505, status: MEDLINE (last retrieved date: 2/18/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Animals Blotting, Western - methods Disease Models, Animal Enzyme Activation - drug effects Focal Adhesion Kinase 2 - metabolism Guanine Nucleotide Exchange Factors - metabolism Hippocampus - drug effects; metabolism Lithium - toxicity Male

Phosphorylation - drug effects Pilocarpine - toxicity Rats Rats, Long-Evans Receptors, N-Methyl-D-Aspartate - classification; genetics; metabolism Status Epilepticus - chemically induced; metabolism Time Factors Tyrosine - metabolism src-Family Kinases - metabolism

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Guanine Nucleotide Exchange Factors (0) ; Psd protein, rat (0) ; Receptors, N-Methyl-D-Aspartate (0) ; Tyrosine (55520-40-6) ; Lithium (7439-93-2) ; Pilocarpine (92-13-7) ; Focal Adhesion Kinase 2 (EC 2.7.1.112) ; src-Family Kinases (EC 2.7.1.112)

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