Modifications by Hypoxia and Drug Treatment of Cerebral ATPase Plasticity

The plasticity of synaptosomal non-mitochondrial ATPases was evaluated in cerebral cortex from 3-month-old normoxic rats and rats subjected to either mild or severe intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10 or 91.5:8.5) for four weeks]. The activities of Na+, K(+)-ATPase, low- and high-affinity Ca(2+)-ATPase, Mg(2+)-ATPase, and Ca2+,Mg(2+)-ATPase were assayed in synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The evaluations were performed after a 4-week treatment with saline (controls) or alpha-adrenergic agents (delta-yohimbine, clonidine), a vasodilator compound (papaverine), and an oxygen-partial pressure increasing agent (almitrine). These treatments differently changed the adaptation to chronic intermittent hypoxia characterized by a decrease in the activity of Na+,K(+)-ATPase, Ca2+,Mg(2+)-ATPase, and high-affinity Ca(2+)-ATPase, concomitant with a modification in the activity of Mg(2+)-ATPase supported in a different way by the enzymatic forms located into the synaptosomal plasma membranes and synaptic vesicles.