Electroconvulsive therapy (ECT) has been used successfully for 70 years to relieve symptoms of major depression. Remarkably, though, precise details about how it acts on the brain to produce this effect was unknown—until NARSAD Young Investigator Grantee Dr. Rupert Lanzenberger and colleagues at the Medical University of Vienna, in Austria, recently performed a series of brain scans on a group of 12 patients.

Their results, published in the journal Molecular Psychiatry this month, show that ECT, like other major forms of antidepressant treatment, acts directly on the function of a class of keyhole-like receptors for the neurotransmitter serotonin. These receptors, one of many subtypes of receptors for serotonin, are called the 5-HT1A, or serotonin 1A receptors. They can be found in many places in the brain, including areas such as the hippocampus, cingulate cortex, and amygdale; these areas help regulate emotion and mood, and are thought to be prime areas in which nerve-cell or circuit dysfunctions involved in depression are centered.

Dr. Lanzenberger’s team performed positron emission tomography (PET) scans on the dozen patients in the study, all of whom met the typical standard for ECT treatment: each had been diagnosed with major depression, and none had achieved remission with a minimum of two antidepressant medications of differing classes. Each patient had two PET scans prior to ECT, while still on medication; and one PET scan a week following treatment with ECT. Ten of the 12, or 83%, experienced a remission. And among these 10, a comparison of before-ECT and after-ECT scans revealed “a widespread reduction” in the binding of the serotonin 1A receptor after treatment, with the greatest changes taking place in those areas just mentioned that are involved in emotional regulation.  

The observed “global decrease” in the binding of the receptors following ECT suggests that this form of antidepressant therapy, when it succeeds, does so for at least some of the same reasons that other treatments succeed, such as SSRI (selective serotonin reuptake inhibitor) antidepressant drugs, such as Paxil (paroxetine), Prozac (fluoxetene), Zoloft (sertraline). The study thus provides further insight into the underlying causes of major depression.

Read the original article from Molecular Phsychiatry