Key result
Electroconvulsive therapy linked to reduced platelet alpha 2-adrenoceptor numbers in depressed patients.
Why the study?
The mechanism of the antidepressant action of electroconvulsive therapy remains unknown, particularly its effects on peripheral adrenoceptor function in depressed patients.
Does electroconvulsive therapy alter peripheral adrenoceptor function and plasma catecholamine/cortisol levels in depressed patients?
Observational (n=36)
Does electroconvulsive therapy alter peripheral adrenoceptor function and plasma catecholamine/cortisol levels in depressed patients?
p-value: p=< 0.03
ECT appears to down-regulate supersensitive platelet alpha 2-adrenoceptors in depressed patients, suggesting a primary normalizing therapeutic effect.
ECT may normalize elevated platelet alpha2-adrenoceptors in depression; leaves open mechanistic role and clinical relevance.
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 alpha 2- and leukocyte beta 2-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 alpha 2-adrenoceptor sites were significantly elevated in untreated patients compared with controls (P < 0.03), but leukocyte beta 2-adrenoceptor numbers did not differ. Treatment with ECT led to a significant reduction in platelet alpha 2-adrenoceptor numbers, whereas leukocyte beta 2-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 beta 2-adrenoceptor numbers were significantly, negatively correlated (P < 0.05). CONCLUSIONS: These results suggest that platelet alpha 2-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 beta 2-adrenoceptors are probably only secondary to the lower circulating plasma NA levels.
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Werstiuk et al. (1996) conducted an observational in Depression (n=36). Electroconvulsive therapy (ECT) vs. Matched control subjects was evaluated on Binding parameters of platelet alpha 2- and leukocyte beta 2-adrenoceptors, plasma NA, MHPG and cortisol levels (p=< 0.03). Electroconvulsive therapy led to a significant reduction in platelet alpha 2-adrenoceptor numbers in depressed patients, which were initially elevated compared with matched controls (P<0.03).
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