RESUMO
Electroconvulsive therapy (ECT) is one of the most effective treatments for treatment-resistant depression. However, this treatment may produce memory impairment. The mechanisms of the cognitive adverse effects are not known. Neuroimmune response is related to the cognitive deficits. By reviewing the available animal literature, we examined the glia activation, inflammatory cytokines, neuron oxidative stress responses, and neural morphological changes following electroconvulsive shock (ECS) treatment. The studies showed that ECS activates microglia, upregulates neuro-inflammatory cytokines, and increases oxidative stress responses. But these effects are rapid and may be transient. They normalize as ECS treatment continues, suggesting endogenous neuroprotection may be mobilized. The transient changes are well in line with the clinical observations that ECT usually does not cause significant long-lasting retrograde amnesia. The longitudinal studies will be particularly important to explore the dynamic changes of neuroplasticity following ECT (Jonckheere et al., 2018). Investigating the neuroplasticity changes in animals that suffered chronic stress may also be crucial to giving support to the translation of preclinical research.
