Depression is a stress-related disorder where, from a clinical perspective, genetic vulnerabilities and environmental factors interact to produce a stressed brain – manifesting as clinical depression. On the other hand, antidepressive interventions such as medication, biological therapies and psychotherapy induce plastic changes which counteract this stressed brain state. Neural plasticity and its positive and negative modulation might be a key element to understand how a brain gets depressed and how depression is relieved.
This symposium examines this concept using a translational approach ranging from molecular neurobiology to clinical trials.
Claus Normann (Freiburg) introduces the neuroplasticity hypothesis of depression and shows the bidirectional modulation of synaptic plasticity in brain slices and animal models of depression caused by stress, antidepressants and brain stimulation, its mechanisms and clinical implications. Igor Branchi (Rome) demonstrates how antidepressants increase neural plasticity. Increased neural plasticity, in turn, enhances the susceptibility to the environment. Therefore, treatment outcome is dependent on the drug by environment interaction. Christoph Nissen (Bern) goes into the assessment of plasticity in healthy and depressed humans and the role of sleep-specific brain activity in the modulation of plasticity. He shows how sleep-specific interventions such as sleep deprivation and non-invasive auditory closed-loop stimulation of slow oscillations in the sleep might be used to treat depression. Martin Walter (Tübingen) focuses on the rapid acting antidepressant ketamine and its effect on brain plasticity. Ketamine might be used to augment psychotherapy; and results from brain imaging will be used to assess this interaction.