Repetitive enhancement of serum BDNF subsequent to continuation ECT.

INTRODUCTION: Continuation electroconvulsive therapy (c-ECT) is highly effective for the prevention of depressive symptom relapse. There is a lack of understanding, about how c-ECT works in humans, particularly with regard to its effects on brain derived neurotrophic factor (BDNF) concentrations. Here, we aimed to close a gap in the literature by evaluating BDNF levels in patients receiving c-ECT. METHODS: We included 13 patients with either unipolar or bipolar depression (mean age ± SD: 55.5 ± 17.1; f/m: 10/3; unipolar/bipolar: 10/3) who received between one and four c-ECT (average per patient: 2.8). Serum BDNF (sBDNF) levels were assessed before and after each c-ECT sessions. Clinical assessments were also administered both before and after treatment. RESULTS: Our analysis revealed a significant increase in sBDNF after each treatment (c-ECT 1-3: P < 0.001, c-ECT 4: P = 0.018). The application of multiple c-ECT treatments was not, however, associated with further sBDNF enhancements. Psychometric scores were not significantly altered following c-ECT. DISCUSSION: An increase in sBDNF concentrations subsequent to c-ECT parallel data from the animal literature, which has linked regularly applied electrical stimulation to neuroplastic processes. This finding suggests a relationship between ECT-induced sBDNF concentrations and (sustained) remission status, considering a stable clinical condition across c-ECT.

Global decrease of serotonin-1A receptor binding after electroconvulsive therapy in major depression measured by PET.

Electroconvulsive therapy (ECT) is a potent therapy in severe treatment-refractory depression. Although commonly applied in psychiatric clinical routine since decades, the exact neurobiological mechanism regarding its efficacy remains unclear. Results from preclinical and clinical studies emphasize a crucial involvement of the serotonin-1A receptor (5-HT(1A)) in the mode of action of antidepressant treatment. This includes associations between treatment response and changes in 5-HT(1A) function and density by antidepressants. Further, alterations of the 5-HT(1A) receptor are consistently reported in depression. To elucidate the effect of ECT on 5-HT(1A) receptor binding, 12 subjects with severe treatment-resistant major depression underwent three positron emission tomography (PET) measurements using the highly selective radioligand [carbonyl-(11)C]WAY100635, twice before (test-retest variability) and once after 10.08±2.35 ECT sessions. Ten patients (~83%) were responders to ECT. The voxel-wise comparison of the 5-HT(1A) receptor binding (BP(ND)) before and after ECT revealed a widespread reduction in cortical and subcortical regions (P<0.05 corrected), except for the occipital cortex and the cerebellum. Strongest reductions were found in regions consistently reported to be altered in major depression and involved in emotion regulation, such as the subgenual part of the anterior cingulate cortex (-27.5%), the orbitofrontal cortex (-30.1%), the amygdala (-31.8%), the hippocampus (-30.6%) and the insula (-28.9%). No significant change was found in the raphe nuclei. There was no significant difference in receptor binding in any region comparing the first two PET scans conducted before ECT. This PET study proposes a global involvement of the postsynaptic 5-HT(1A) receptor binding in the effect of ECT.