Document Detail


Loss of perivascular Kir4.1 potassium channels in the sclerotic hippocampus of patients with mesial temporal lobe epilepsy.
MedLine Citation:
PMID:  22878665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent experimental data in mice have shown that the inwardly rectifying K channel Kir4.1 mediates K spatial buffering in the hippocampus. Here we used immunohistochemistry to examine the distribution of Kir4.1 in hippocampi from patients with medication-refractory temporal lobe epilepsy. The selectivity of the antibody was confirmed in mice with a glial conditional deletion of the gene encoding Kir4.1. These mice showed a complete loss of labeled cells, indicating that Kir4.1 is restricted to glia. In human cases, Kir4.1 immunoreactivity observed in cells morphologically consistent with astrocytes was significantly reduced in 12 patients with hippocampal sclerosis versus 11 patients without sclerosis and 4 normal autopsy controls. Loss of astrocytic Kir4.1 immunoreactivity was most pronounced around vessels and was restricted to gliotic areas. Loss of Kir4.1 expression was associated with loss of dystrophin and α-syntrophin, but not with loss of β-dystroglycan, suggesting partial disruption of the dystrophin-associated protein complex. The changes identified in patients with hippocampal sclerosis likely interfere with K homeostasis and may contribute to the epileptogenicity of the sclerotic hippocampus.
Authors:
Kjell Heuser; Tore Eid; Fredrik Lauritzen; Anna E Thoren; Gry F Vindedal; Erik Taubøll; Leif Gjerstad; Dennis D Spencer; Ole P Ottersen; Erlend A Nagelhus; Nihal C de Lanerolle
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuropathology and experimental neurology     Volume:  71     ISSN:  1554-6578     ISO Abbreviation:  J. Neuropathol. Exp. Neurol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-28     Completed Date:  2012-11-02     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  2985192R     Medline TA:  J Neuropathol Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  814-25     Citation Subset:  IM    
Affiliation:
Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Age Factors
Animals
Animals, Newborn
Calcium-Binding Proteins / metabolism
Child
Dystroglycans / metabolism
Dystrophin / metabolism
Epilepsy, Temporal Lobe / complications,  pathology*
Female
Gene Expression Regulation / physiology*
Hippocampus / metabolism*,  pathology
Humans
Male
Membrane Proteins / metabolism
Mice
Mice, Knockout
Middle Aged
Muscle Proteins / metabolism
Neuroglia / metabolism
Potassium Channels, Inwardly Rectifying / metabolism*
Sclerosis / etiology*,  pathology
Young Adult
Grant Support
ID/Acronym/Agency:
K08 NS058674/NS/NINDS NIH HHS; NS058674/NS/NINDS NIH HHS; NS070824/NS/NINDS NIH HHS; R01 NS070824/NS/NINDS NIH HHS; UL1 RR024139/RR/NCRR NIH HHS; UL1 RR024139/RR/NCRR NIH HHS; UL1 TR000142/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Dystrophin; 0/Membrane Proteins; 0/Muscle Proteins; 0/Potassium Channels, Inwardly Rectifying; 0/potassium inwardly-rectifying channel, subfamily J, member 10; 0/syntrophin alpha1; 146888-27-9/Dystroglycans
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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