摘要Background::Synchronization across neural circuits is inextricably associated with brain function and pathology. Although not largely explored, this framework can be applied to baseline anxiety and its disorder, which is characterized by aberrant levels of synchronization between the amygdala nuclei and other areas of the extended amygdala, particularly the bed nucleus of the stria terminalis (BNST) and those outside this complex. Here, we aimed to test the hypothesis that a temporally complex form of electrical stimulation (non-periodic stimulation [NPS]) of the amygdala, specifically designed to disrupt hypersynchronous activity in epilepsy, a major comorbidity of pathological anxiety, may reduce its symptoms.Methods::Wistar rats were subjected to a physical restriction protocol model of stress to induce pathological anxiety and were assessed using the gold standard elevated plus maze (EPM) and open field (OF) tests.Result::In all criteria measured by the tests, NPS animals displayed reduced levels of anxiety-related symptoms, back at physiological levels.Conclusions::Considering the known effects and mechanisms of NPS on epileptic phenomena, we hypothesized that the therapeutic effects were achieved by desynchronization (or normalization of synchronism levels) across brain circuits involving the amygdala, BNST, and others. Overall, past and present findings suggest that NPS may be considered as a therapeutic alternative for the treatment of anxiety disorders.