Changes in Na+, K+-ATPase activity and alpha 3 subunit expression in CNS after administration of Na+, K+-ATPase inhibitors

M. G. BERSIER; C. PEÑA ; G. RODRÍGUEZ DE LORES ARNAIZ (

NEUROCHEMICAL RESEARCH

SPRINGER/PLENUM PUBLISHERS

Año: 2011 vol. 36 p. 297 - 303

0364-3190

The expression of Na?, K?-ATPase a3 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 a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, K?-ATPase a3 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 a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, 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 a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, 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 a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?-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 a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, K?-ATPase a3 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 ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.ll endobain E (1 ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.ll = 28 mg tissue) Na?, K?-ATPase a3 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, 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 a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, K?-ATPase inhibitors modify differentially the expression of Na?, K?-ATPase a3 subunit and enzyme activity, most likely involving compensatory mechanisms.?, K?-ATPase a3 subunit and enzyme activity, most likely involving compensatory mechanisms. Keywords Na?, K?-ATPase inhibitors Na?, K?- ATPase activity Na?, K?-ATPase a3 Subunit Na?, K?-ATPase inhibitors Na?, K?- ATPase activity Na?, K?-ATPase a3 Subunit Na?, K?-ATPase a3 Subunit