Synaptosomal non-mitochondrial ATPase activities and drug treatment.

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Benzi G, Gorini A, Ghigini B, Arnaboldi R, Villa RF

Synaptosomal non-mitochondrial ATPase activities and drug treatment.

Neurochem Res. 1993 Jun;18(6):719-26.

PubMed ID

8099718 [ View in PubMed

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Abstract

Energy-using non-mitochondrial ATPases were assayed in rat cerebral cortex synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The following enzyme activities were evaluated: Na+, K+ -ATPase; high- and low-affinity Ca2+ -ATPase; basal Mg(2+)-ATPase; Ca2+, Mg(2+)-ATPase. The evaluations were performed after four week-treatment with saline [controls] or alpha-adrenergic agents (delta-yohimbine, clonidine), energy-metabolism interfering compound (theniloxazine), and oxygen-partial pressure increasing agent (almitrine), in order to define the plasticity and the selective changes in individual ATPases. In rat cerebral cortex, the enzyme adaptation to four-week-treatment with delta-yohimbine or clonidine was characterized by increase in both high- and low-affinity Ca2+ -ATPase activities. The action involves the enzyme form located in the synaptic plasma membranes. The enzyme adaptation to the subchronic treatments with theniloxazine or almitrine was characterized by increase in Na+, K(+)-ATPase or Mg(2+)-ATPase activities, respectively. The action involves the enzymatic forms located in the synaptic plasma membranes. Thus, the pharmacodynamic effects of the agents tested should also be related to the changes induced in the activity of some specific synaptosomal non-mitochondrial ATPases.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Almitrine	Sodium/potassium-transporting ATPase subunit alpha-1	Protein	Humans	Yes	Binder	Details