Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0038220 (
status epilepticus
)
7,272
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Loss of intracellular calcium homeostasis is an established mechanism associated with neuronal dysfunction and
status epilepticus
. Sequestration of free cytosolic calcium into endoplasmic reticulum by Mg
2+
/Ca
2+
adenosinetriphosphatase
(
ATPase
) is critical for maintenance of intracellular calcium homeostasis. Exposing hippocampal cultures to low-magnesium media is a well-accepted in vitro model of
status epilepticus
. Using this model, it was shown that endoplasmic reticulum Ca
2+
uptake was significantly inhibited in homogenates from cultures demonstrating electrophysiological seizure phenotypes. Calcium uptake was mainly neuronal. However, glial Ca
2+
uptake was also significantly inhibited. Viability of neurons exposed to low magnesium was similar to neurons exposed to control solutions. Finally, it was demonstrated that Ca
2+
uptake inhibition and intracellular free Ca
2+
levels increased in parallel with increasing incubation in low magnesium. The results suggest that inhibition of Mg
2+
/Ca
2+
ATPase
-mediated endoplasmic reticulum Ca
2+
sequestration contributes to loss of intracellular Ca
2+
homeostasis associated with
status epilepticus
. This study describes for the first time inhibition of endoplasmic reticulum Mg
2+
/Ca
2+
ATPase
in a mixed primary hippocampal model of
status epilepticus
. In combination with animal models of
status epilepticus
, the cell culture model provides a powerful tool to further elucidate mechanisms that result in inhibition of Mg
2+
/Ca
2+
ATPase
and downstream consequences of decreased enzyme activity.
...
PMID:Neuronal-Specific Inhibition of Endoplasmic Reticulum Mg
2+
/Ca
2+
ATPase Ca
2+
Uptake in a Mixed Primary Hippocampal Culture Model of Status Epilepticus. 3266 97
