Localization of ATPase activity in dendritic spines of the cerebral cortex

1991 ◽  
Vol 20 (9) ◽  
pp. 703-715 ◽  
Author(s):  
R. S. Cohen ◽  
V. Kriho
Keyword(s):  
Cerebral Cortex ◽  
Atpase Activity ◽  
Dendritic Spines

Role of antioxidants on Na+,K+-ATPase activity and gene expression in cerebral cortex of hyperprolinemic rats

2011 ◽  
Vol 26 (2) ◽  
pp. 141-147 ◽  
Author(s):  
Andréa G. K. Ferreira ◽  
Francieli M. Stefanello ◽  
Aline A. Cunha ◽  
Maira J. da Cunha ◽  
Talita C. B. Pereira ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Atpase Activity

scholarly journals Mechanisms of L-Triiodothyronine-Induced Inhibition of Synaptosomal Na+-K+-ATPase Activity in Young Adult Rat Brain Cerebral Cortex

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Pradip K. Sarkar ◽  
Avijit Biswas ◽  
Arun K. Ray ◽  
Joseph V. Martin
Keyword(s):  
Cerebral Cortex ◽  
Atpase Activity ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Mammalian Brain ◽  
Neuronal Membrane ◽  
Dependent Manner ◽  
Adrenergic Agonist ◽  
Adult Rat ◽  
Dose Dependent

The role of thyroid hormones (TH) in the normal functioning of adult mammalian brain is unclear. Our studies have identified synaptosomal Na+-K+-ATPase as a TH-responsive physiological parameter in adult rat cerebral cortex. L-triiodothyronine (T3) and L-thyroxine (T4) both inhibited Na+-K+-ATPase activity (but not Mg2+-ATPase activity) in similar dose-dependent fashions, while other metabolites of TH were less effective. Although both T3and theβ-adrenergic agonist isoproterenol inhibited Na+-K+-ATPase activity in cerebrocortical synaptosomes in similar ways, theβ-adrenergic receptor blocker propranolol did not counteract the effect of T3. Instead, propranolol further inhibited Na+-K+-ATPase activity in a dose-dependent manner, suggesting that the effect of T3on synaptosomal Na+-K+-ATPase activity was independent ofβ-adrenergic receptor activation. The effect of T3on synaptosomal Na+-K+-ATPase activity was inhibited by theα2-adrenergic agonist clonidine and by glutamate. Notably, both clonidine and glutamate activateGi-proteins of the membrane second messenger system, suggesting a potential mechanism for the inhibition of the effects of TH. In this paper, we provide support for a nongenomic mechanism of action of TH in a neuronal membrane-related energy-linked process for signal transduction in the adult condition.

Inhibition of purified (Na+,K+)-ATPase activity from porcine cerebral cortex by NO generating drugs

1995 ◽  
Vol 704 (1) ◽  
pp. 117-120 ◽  
Author(s):  
Tomoaki Sato ◽  
Yoshiko Kamata ◽  
Masahiro Irifune ◽  
Takashige Nishikawa
Keyword(s):  
Cerebral Cortex ◽  
Atpase Activity

Effects of postnatal steroids on Na+/K+-ATPase activity and α1- and β1-subunit protein expression in the cerebral cortex and renal cortex of newborn lambs

2006 ◽  
Vol 18 (4) ◽  
pp. 413 ◽  
Author(s):  
Chang-Ryul Kim ◽  
Grazyna B. Sadowska ◽  
Katherine H. Petersson ◽  
Maricruz Merino ◽  
Gregory D. Sysyn ◽  
...  
Keyword(s):  
At Risk ◽  
Cerebral Cortex ◽  
Protein Expression ◽  
Atpase Activity ◽  
Renal Cortex ◽  
Newborn Infants ◽  
Electrolyte Balance ◽  
Dexamethasone Treatment ◽  
Protein Isoform ◽  
Isoform Expression

Na+/K+-ATPase is a membrane-bound enzyme responsible for Na+/K+ translocation across cell membranes. It is essential for the generation of electrochemical gradients, which control the ionic environment necessary for electrical activity and water and electrolyte balance. Newborn infants who are at risk of developing bronchopulmonary dysplasia (BPD) are frequently treated with corticosteroids. Although these infants are at risk for neurological, water and electrolyte abnormalities, there is little information regarding the effects of clinically relevant doses of corticosteroids on Na+/K+-ATPase activity and protein isoform expression in the brain and kidney of newborns. In the present study, we examined the effects of dexamethasone on cerebral cortical and renal cortical Na+/K+-ATPase activity and α1- and β1-protein isoform expression in newborn lambs. Lambs were given four injections of a placebo (n = 11) or one of three different doses of dexamethasone (0.01 mg kg−1, n = 9; 0.25 mg kg−1, n = 11; or 0.50 mg kg−1, n = 9) 12 h apart on Postnatal Days 3 and 4 up to 18 h before harvest of the cerebral cortex and renal cortex. We selected doses in a range to approximate those used to treat infants with BPD. Na+/K+-ATPase activity was measured in membrane preparations as ouabain-sensitive inorganic phosphate liberation from ATP and α1- and β1-subunit abundance by Western immunoblot. Postnatal treatment of lambs with dexamethasone resulted in a 21.4% increase in Na+/K+-ATPase activity and a 30.4% increase in catalytic α1-protein expression in the cerebral cortex at a dose of 0.50 mg kg−1 dexamethasone, but not at the lower doses. Dexamethasone treatment was not associated with changes in β1-isoform expression in the cerebral cortex. In the kidney, dexamethasone treatment was not associated with significant changes in Na+/K+-ATPase activity or α1- or β1-isoform expression for the doses we examined. Therefore, clinically relevant corticosteroid treatment exerts dose-related, differential organ-specific effects on Na+/K+-ATPase activity and protein isoform expression in newborn lambs.

(Na+, K+)-ATPase regulation and NaCl intake: effects on circulating inhibitor and sensitivity to noradrenaline

1985 ◽  
Vol 69 (4) ◽  
pp. 441-447 ◽  
Author(s):  
Alan C. Swann
Keyword(s):  
Cerebral Cortex ◽  
Plasma Level ◽  
Atpase Activity ◽  
Ouabain Binding ◽  
Kidney Medulla ◽  
High Salt Diet ◽  
Salt Diet ◽  
Amphetamine Administration ◽  
Inhibitor Level ◽  
Stimulation Of

1. These experiments examined the effects of a high NaCl diet on (Na+, K+)-ATPase in kidney, heart and cerebral cortex, on the level of circulating inhibitor of (Na+, K+)-ATPase in plasma, and on stimulation of (Na+, K+)-ATPase by treatment with dextro (d)-amphetamine. 2. High salt diet increased indices of (Na+, K+)-ATPase activity (K+-activated p-nitrophenylphosphatase activity and ouabain binding) in kidney medulla, prevented stimulation by amphetamine in cerebral cortex and reduced amphetamine stimulation in heart. 3. High NaCl feeding increased the plasma level of circulating inhibitor of (Na+, K+)-ATPase. 4. Amphetamine alone had no effect on inhibitor level but amphetamine administration reduced the increase in inhibitor with high NaCl feeding.

Sign in / Sign up

Export Citation Format

Share Document