Electroconvulsive Shock Induces Greater Plasticity of Dentate Gyrus Neurons Born in Adulthood Than Those Born in Development

Electroconvulsive therapy (ECT) is the most effective treatment for severe depression but uptake is hindered due to effects on memory and a poor understanding of its mechanisms of action. Hippocampal plasticity is one consequence of ECT that may be related to both the therapeutic and amnestic effects. In animals, electroconvulsive shock (ECS) dramatically increases adult neurogenesis in the dentate gyrus (DG). However, little is known about how ECS impacts the morphology of adult‐born neurons. Moreover, it is unknown whether ECS differentially impacts DG neurons that are born in development versus adulthood. To address these questions, here, we subjected male and female mice to a clinically relevant schedule of chronic ECS and examined effects on DG neuron populations. As predicted, ECS dramatically increased the survival of adult‐born DG neurons generated shortly before treatment and the number of immature neurons present after treatment. Adult‐born neurons from ECS‐treated mice also had longer dendrites and larger presynaptic terminals, suggesting enhanced circuit integration. In contrast, ECS did not affect the survival of neurons born in early postnatal development and it did not alter the structure of their dendrites or presynaptic terminals. Instead, ECS reduced spine density on developmentally born neurons in the dorsal DG and, in the ventral DG, it increased mushroom spine density. Thus, adult‐born neurons generally display greater ECS‐induced plasticity than developmentally born neurons, which may be relevant for the effects of ECS/ECT on cognition and mood.