RGD Reference Report - Calcium extrusion protein expression in the hippocampal formation of chronic epileptic rats after kainate-induced status epilepticus. - Rat Genome Database

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Calcium extrusion protein expression in the hippocampal formation of chronic epileptic rats after kainate-induced status epilepticus.

Authors: Ketelaars, SO  Gorter, JA  Aronica, E  Wadman, WJ 
Citation: Ketelaars SO, etal., Epilepsia. 2004 Oct;45(10):1189-201.
RGD ID: 2316980
Pubmed: PMID:15461673   (View Abstract at PubMed)
DOI: DOI:10.1111/j.0013-9580.2004.03304.x   (Journal Full-text)

PURPOSE: The plasma membrane Ca2+ -adenosine triphosphatase (ATPase) (PMCA) and (potassium-dependent) sodium-calcium exchange [NC(K)X] represent two main calcium-extrusion mechanisms that are important for the restoration of [Ca2+]i levels after electrical activity. We investigated whether the expression of these calcium-extrusion proteins is altered in the course of epileptogenesis. METHODS: Hippocampal-parahippocampal protein expression of NCX1, 2, and 3, PMCA1-4, and NCKX2 at an early and late stage after kainate-induced status epilepticus (SE) was compared with that in control rats by using immunocytochemistry. RESULTS: Several alterations were found in chronic epileptic rats: (a) NCX1 expression was permanently decreased in the inner molecular layer (IML) of the dentate gyrus (DG) and entorhinal cortex layer III (ECIII), related to neuronal loss in hilus and ECIII, respectively; (b) PMCA and NCKX2 expression was transiently upregulated in the IML, and decreased in several areas where cell loss had occurred, (c) NCX3 expression, which in control rats is abundant in presynaptic terminals of mossy fibers (MF), was extensively and permanently decreased in stratum lucidum and hilar region. In addition, newly formed MF sprouts that project to the DG iml did not noticeably express NCX3; (d) NCX2 and NCKX2 were (transiently) upregulated in astrocytes of epileptic rats throughout the hippocampal formation, including ECIII. CONCLUSIONS: These region-specific changes in calcium-extrusion proteins reflect a change in calcium regulation. Whether these regional-specific changes of calcium-extrusion proteins are associated with an abnormal calcium homeostasis must be determined. Because some alterations of calcium-extrusion protein expression are already present at an early stage of epileptogenesis, they could be involved in this process.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SLC8A1Humanstatus epilepticus  ISOSlc8a1 (Rattus norvegicus)protein:decreased expression:brainRGD 
SLC8A2Humanstatus epilepticus  ISOSlc8a2 (Rattus norvegicus) RGD 
SLC8A3Humanstatus epilepticus  ISOSlc8a3 (Rattus norvegicus)protein:decreased expression:brainRGD 
Slc8a1Ratstatus epilepticus  IEP protein:decreased expression:brainRGD 
Slc8a1Mousestatus epilepticus  ISOSlc8a1 (Rattus norvegicus)protein:decreased expression:brainRGD 
Slc8a2Ratstatus epilepticus  IEP  RGD 
Slc8a2Mousestatus epilepticus  ISOSlc8a2 (Rattus norvegicus) RGD 
Slc8a3Ratstatus epilepticus  IEP protein:decreased expression:brainRGD 
Slc8a3Mousestatus epilepticus  ISOSlc8a3 (Rattus norvegicus)protein:decreased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Slc8a1  (solute carrier family 8 member A1)
Slc8a2  (solute carrier family 8 member A2)
Slc8a3  (solute carrier family 8 member A3)

Genes (Mus musculus)
Slc8a1  (solute carrier family 8 (sodium/calcium exchanger), member 1)
Slc8a2  (solute carrier family 8 (sodium/calcium exchanger), member 2)
Slc8a3  (solute carrier family 8 (sodium/calcium exchanger), member 3)

Genes (Homo sapiens)
SLC8A1  (solute carrier family 8 member A1)
SLC8A2  (solute carrier family 8 member A2)
SLC8A3  (solute carrier family 8 member A3)


Additional Information