Global decrease of serotonin-1A receptor binding after electroconvulsive therapy in major depression measured by PET.
ABSTRACT 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.Molecular Psychiatry advance online publication, 3 July 2012; doi:10.1038/mp.2012.93.
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ABSTRACT: The serotonin syndrome has been described only in rare instances for electroconvulsive therapy combined with an antidepressant medication. We describe a case of serotonin toxicity induced by electroconvulsive therapy in combination with fluoxetine.Case reports in psychiatry. 01/2014; 2014:162502.
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ABSTRACT: Aim of this work was the implementation of a generalized in-loop synthesis for 11C-carboxylations and subsequent 11C-acylations on the TRACERlab FxC Pro platform. The set-up was tested using [carbonyl-11C]WAY-100635 and, for the first time, [11C]-(+)-PHNO. Its general applicability could be demonstrated and both [carbonyl-11C]WAY-100635 and [11C]-(+)-PHNO were prepared with high reliability and satisfying outcome.Applied Radiation and Isotopes. 01/2013; 82:75–80.
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ABSTRACT: Depressive disorder is frequently accompanied by changes in psychomotor activity and disturbances of the sleep-wake cycle. The chronobiological effects of electroconvulsive therapy (ECT) in patients with treatment-resistant depression (TRD) are largely unknown. The objective of the current study was to measure the influence of ECT on patients’ activity and sleep. 15 patients with unipolar TRD were treated with ECT. Activity levels were measured with wrist actigraphy before and after ECT. Remission rate (score on the 17-item Hamilton Depression Rating Scale lower than 8 points) was 40.0%. Remitters had increases of 56.0% on light activity, 49.8% on total activity, and 70.2% on circadian amplitude, while there was no significant change of these variables in subjects who did not experience remission. The circadian acrophase and actigraphic sleep-parameters were not significantly affected by treatment.Journal of Psychiatric Research. 01/2014;