Changes in Na+, K+-ATPase Activity and Alpha 3 Subunit Expression in CNS After Administration of Na+, K+-ATPase Inhibitors

The expression of Na + , K + -ATPase α3 subunit and synaptosomal membrane Na + , K + -ATPase activity were analyzed after administration of ouabain and endobain E, respectively commercial and endogenous Na + , K + -ATPase inhibitors. Wistar rats received intracerebroventricularly ouabain or endobain...

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Published in:Neurochemical research Vol. 36; no. 2; pp. 297 - 303
Main Authors: Bersier, María Geraldina, Peña, Clara, Rodríguez de Lores Arnaiz, Georgina
Format: Journal Article
Language:English
Published: Boston Springer US 01-02-2011
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Abstract The expression of Na + , K + -ATPase α3 subunit and synaptosomal membrane Na + , K + -ATPase activity were analyzed after administration of ouabain and endobain E, respectively commercial and endogenous Na + , K + -ATPase inhibitors. Wistar rats received intracerebroventricularly ouabain or endobain E dissolved in saline solution or Tris–HCl, respectively or the vehicles (controls). Two days later, animals were decapitated, cerebral cortex and hippocampus removed and crude and synaptosomal membrane fractions were isolated. Western blot analysis showed that Na + , K + -ATPase α3 subunit expression increased roughly 40% after administration of 10 or 100 nmoles ouabain in cerebral cortex but remained unaltered in hippocampus. After administration of 10 μl endobain E (1 μl = 28 mg tissue) Na + , K + -ATPase α3 subunit enhanced 130% in cerebral cortex and 103% in hippocampus. The activity of Na + , K + -ATPase in cortical synaptosomal membranes diminished or increased after administration of ouabain or endobain E, respectively. It is concluded that Na + , K + -ATPase inhibitors modify differentially the expression of Na + , K + -ATPase α3 subunit and enzyme activity, most likely involving compensatory mechanisms.
AbstractList The expression of Na(+), K(+)-ATPase α3 subunit and synaptosomal membrane Na(+), K(+)-ATPase activity were analyzed after administration of ouabain and endobain E, respectively commercial and endogenous Na(+), K(+)-ATPase inhibitors. Wistar rats received intracerebroventricularly ouabain or endobain E dissolved in saline solution or Tris-HCl, respectively or the vehicles (controls). Two days later, animals were decapitated, cerebral cortex and hippocampus removed and crude and synaptosomal membrane fractions were isolated. Western blot analysis showed that Na(+), K(+)-ATPase α3 subunit expression increased roughly 40% after administration of 10 or 100 nmoles ouabain in cerebral cortex but remained unaltered in hippocampus. After administration of 10 μl endobain E (1 μl = 28 mg tissue) Na(+), K(+)-ATPase α3 subunit enhanced 130% in cerebral cortex and 103% in hippocampus. The activity of Na(+), K(+)-ATPase in cortical synaptosomal membranes diminished or increased after administration of ouabain or endobain E, respectively. It is concluded that Na(+), K(+)-ATPase inhibitors modify differentially the expression of Na(+), K(+)-ATPase α3 subunit and enzyme activity, most likely involving compensatory mechanisms.
The expression of Na + , K + -ATPase α3 subunit and synaptosomal membrane Na + , K + -ATPase activity were analyzed after administration of ouabain and endobain E, respectively commercial and endogenous Na + , K + -ATPase inhibitors. Wistar rats received intracerebroventricularly ouabain or endobain E dissolved in saline solution or Tris–HCl, respectively or the vehicles (controls). Two days later, animals were decapitated, cerebral cortex and hippocampus removed and crude and synaptosomal membrane fractions were isolated. Western blot analysis showed that Na + , K + -ATPase α3 subunit expression increased roughly 40% after administration of 10 or 100 nmoles ouabain in cerebral cortex but remained unaltered in hippocampus. After administration of 10 μl endobain E (1 μl = 28 mg tissue) Na + , K + -ATPase α3 subunit enhanced 130% in cerebral cortex and 103% in hippocampus. The activity of Na + , K + -ATPase in cortical synaptosomal membranes diminished or increased after administration of ouabain or endobain E, respectively. It is concluded that Na + , K + -ATPase inhibitors modify differentially the expression of Na + , K + -ATPase α3 subunit and enzyme activity, most likely involving compensatory mechanisms.
Author Peña, Clara
Bersier, María Geraldina
Rodríguez de Lores Arnaiz, Georgina
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  surname: Bersier
  fullname: Bersier, María Geraldina
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  givenname: Clara
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  givenname: Georgina
  surname: Rodríguez de Lores Arnaiz
  fullname: Rodríguez de Lores Arnaiz, Georgina
  email: grodrig@ffyb.uba.ar
  organization: Instituto de Biología Celular y Neurociencias “Prof. E. De Robertis”, CONICET-UBA, Facultad de Medicina and Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Instituto de Biología Celular y Neurociencias “Prof. E. De Robertis”, CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires
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Issue 2
Keywords Endobain E
Na
ATPase activity
Expression
ATPase
Ouabain
ATPase inhibitors
K
α3 Subunit
Language English
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Snippet The expression of Na + , K + -ATPase α3 subunit and synaptosomal membrane Na + , K + -ATPase activity were analyzed after administration of ouabain and...
The expression of Na(+), K(+)-ATPase α3 subunit and synaptosomal membrane Na(+), K(+)-ATPase activity were analyzed after administration of ouabain and...
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SubjectTerms Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Central Nervous System - drug effects
Central Nervous System - metabolism
Enzyme Inhibitors - pharmacology
Male
Neurochemistry
Neurology
Neurosciences
Original Paper
Ouabain - analogs & derivatives
Ouabain - pharmacology
Rats
Rats, Wistar
Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
Sodium-Potassium-Exchanging ATPase - metabolism
Synaptosomes - drug effects
Synaptosomes - enzymology
Title Changes in Na+, K+-ATPase Activity and Alpha 3 Subunit Expression in CNS After Administration of Na+, K+-ATPase Inhibitors
URI https://link.springer.com/article/10.1007/s11064-010-0317-x
https://www.ncbi.nlm.nih.gov/pubmed/21080065
https://search.proquest.com/docview/845765288
Volume 36
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