Repeated electroconvulsive shock induces changes in high-affinity [H-3]-ouabain binding to rat striatal membranes

Abstract

Repeated electroconvulsive shock is an effective treatment for affective disorders. Striatum, hippocampus and brainstem are involved in affective disorders. Sodium-potassium/ATPase is of paramount importance for the proper functioning of the brain and its involvement in the affective disorders has been claimed for a long time. Sodium-potassium/ATPase has an extracellular regulatory binding site to which cardiotonic glycosides, such as ouabain, bind to, thus regulating the activity of the enzyme. Endogenous ouabain-like substances exist in the brain and their actions on the sodium-potassium/ATPase resemble ouabain biological properties. the aim of this work was to determine if electroconvulsive shock (ECS) would induce changes in the high-affinity binding of ouabain to the sodium-potassium/ATPase from rat brain regions. Adult, male Wistar rats received one (ECSx1 group) or seven electroshocks (ECSx7 group) delivered daily through ear-clips electrodes. Control rats received the same manipulations; however, no current was delivered through the electrodes (SHAMx1 and SHAMx7 groups). All groups were sacrificed 24 h after the last ECS session. the B-max and K-D of high-affinity [3H]-ouabain binding were determined in crude membrane preparations from the striatum, hippocampus and brainstem. the results obtained showed a statistically significant increase in the affinity of [H-3]-ouabain (lower K (D)) to striatal membranes in those rats receiving seven ECS. in the striatum there was no change in the K (D) after one ECS; as well as there was no change in the B-max after a single or seven ECS. High-affinity [H-3]-ouabain binding to hippocampus and brainstem did not reveal any significant differences either in K (D) or B-max after one or seven ECS. the increased affinity of ouabain to the striatal sodium-potassium/ATPase induced by repeated ECS suggests an increased interaction in vivo of the endogenous ouabain-like substances with the enzyme and the involvement of the extracellular regulatory allosteric ouabain binding site in the striatal sodium-potassium/ATPase in the effects of electroconvulsive shock.