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Effects of Electroconvulsive Therapy on Peripheral Adrenoceptors, Plasma, Noradrenaline, MHPG and Cortisol in Depressed Patients

Published online by Cambridge University Press:  02 January 2018

Eva S. Werstiuk
Affiliation:
Department of Biomedical Sciences, McMaster University, Hamilton
Margaret Coote
Affiliation:
Departments of Biomedical Sciences and Psychiatry, McMaster University and St Joseph's Hospital, Hamilton
Lauren Griffith
Affiliation:
Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton
Harry Shannon
Affiliation:
Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton
Meir Steiner*
Affiliation:
Departments of Psychiatry and Biomedical Sciences, McMaster University, and Department of Psychiatry, St Joseph's Hospital, Hamilton
*
Dr Meir Steiner, Chief and Clinical Director, Department of Psychiatry, St Joseph's Hospital, 50 Charlton Avenue East, Hamilton, Ontario L8N 4A6, Canada. Fax: (905) 521–6098

Abstract

Background

The mechanism of the antidepressant action of electroconvulsive therapy (ECT) remains unknown. Based on previous work with antidepressant drugs and their effects on the noradrenergic system, we undertook this study to further determine the effects of ECT on selected indices of peripheral adrenoceptor function in depressed patients.

Methods

Binding parameters (Bmax and Kd) of platelet α2- and leukocyte β2-adrenoceptors, plasma noradrenaline (NA), 3-methoxy-4-hydroxy-phenylglycol (MHPG) and cortisol levels were determined in 18 patients, prior to treatment and 14 days after the last of a series of ECTs, and compared with samples obtained from 18 matched control subjects.

Results

Platelet α2-adrenoceptor sites were significantly elevated in untreated patients compared with controls (P < 0.03), but leukocyte β2-adrenoceptor numbers did not differ. Treatment with ECT led to a significant reduction in platelet α2-adrenoceptor numbers, whereas leukocyte β2-adrenoceptor densities increased. Pre-ECT plasma NA, MHPG, and cortisol levels were elevated in patients, compared with controls, and decreased following ECT, but these differences were not statistically significant. Post-ECT plasma NA and β2-adrenoceptor numbers were significantly, negatively correlated (P < 0.05).

Conclusions

These results suggest that platelet α2-adrenoceptors are supersensitive in depressed patients and treatment with ECT results in down-regulation of these receptors, which may be interpreted as a primary therapeutic, ‘normalising’ effect. The post-ECT changes in leukocyte β2-adrenoceptors are probably only secondary to the lower circulating plasma NA levels.

Type
Papers
Copyright
Copyright © 1996 The Royal College of Psychiatrists 

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