Effect of in vivo administration of naloxone on ATP-ase's enzyme systems of synaptic plasma membranes from rat cerebral cortex

Naloxone is a specific competitive antagonist of morphine, acting on opiate receptors, located on neuronal membranes. The effects of in vivo administration of naloxone on energy-consuming non-mitochondrial ATP-ases were studied in two different types of synaptic plasma membranes from rat cerebral cortex, known to contain a high density of opiate receptors. The enzyme activities of Na+, K(+)-ATP-ase, Ca(2+), Mg(2+)-ATP-ase and Mg(2+)-ATP-ase and of acetylcholinesterase (AChE) were evaluated on synaptic plasma membranes obtained from control and treated animals with effective dose of naloxone (12microg x kg(-1) i.m. 30 minutes). In control (vehicle-treated) animals specific enzyme activities assayed on these two types of synaptic plasma membranes are different, being higher on synaptic plasma membranes of II type than of I type, because the first fraction is more enriched in synaptic plasma membranes. The acute treatment with naloxone produced a significant decrease in Ca(2+),Mg(2+)-ATP-ase activity and an increase in AChE activity, only in synaptic plasma membranes of II type. The decrease of Ca(2+), Mg(2+)-ATP-ase enzymatic activity and the increased AChE activity are related to the interference of the drug on Ca(2+) homeostasis in synaptosoplasm, that leads to the activation of calcium-dependent processes, i.e. the extrusion of neurotransmitter. These findings give further evidence that pharmacodynamic characteristics of naloxone are also related to increase [Ca(2+)]i, interfering with enzyme systems (Ca(2+), Mg(2+)-ATP-ase) and that this drug increases acetylcholine catabolism in synaptic plasma membranes of cerebral corte