Electroconvulsive therapy alters dopamine signaling in the striatum of non-human primates.

Electroconvulsive therapy (ECT) is one of the most effective therapies for depression and has beneficial motor effects in parkinsonian patients. However, little is known about the mechanisms of therapeutic action of ECT for either condition. The aim of this work was to explore the impact of ECT on dopaminergic function in the striatum of non-human primates.

Effect of electroconvulsive therapy on brain 5-HT(2) receptors in major depression.

Background: Brain serotonin(2) (5-hydroxytryptamine(2); 5-HT(2)) receptors were considered potential targets for therapeutic efficacy of electroconvulsive therapy (ECT), but pre-clinical studies showed that electroconvulsive shock up-regulates 5-HT(2) receptors in contrast to antidepressant medications, which down-regulate brain 5-HT(2) receptors. Positron emission tomography (PET) studies in individuals with depression confirmed that antidepressant medications reduce brain 5-HT(2) receptors, but the effects of ECT on these receptors in individuals with depression are unknown.

Aims: To determine if a course of ECT alters brain 5-HT(2) receptors in individuals with depression and whether such changes correlate with improvement in symptoms.

Electroconvulsive shock enhances striatal dopamine D1 and D3 receptor binding and improves motor performance in 6-OHDA-lesioned rats.

Objective: Electroconvulsive therapy (ECT) is a widely used and effective treatment for mood disorders and appears to have positive effects on the motor symptoms of Parkinson's disease (PD), improving motor function for several weeks. Because repeated electroconvulsive shock (ECS) in normal animals enhances striatal dopamine (DA) D(1) and D(3) receptor binding, we hypothesized that upregulation of D(1) and D(3) receptors may also be occurring in the parkinsonian brain after repeated ECS treatment.

Methods: Rats were rendered hemi-parkinsonian through unilateral infusion of the DA-specific neurotoxin 6-hydroxydopamine into the medial forebrain bundle and substantia nigra.

Electroconvulsive shock decreases binding to 5-HT2 receptors in nonhuman primates: an in vivo positron emission tomography study with [18F]setoperone.

Background: Dysfunction within the serotonin (5-HT) system plays a major role in the etiology of human depression, and treatment with antidepressant drugs downregulates 5-HT(2) receptors in rodents and humans. The consequences of another effective antidepressant treatment, electroconvulsive therapy (ECT), on 5-HT(2) receptors are less established.

Methods: We studied the effects of a course of electroconvulsive shock (ECS) on 5-HT(2) receptor binding in nonhuman primates in vivo using positron emission tomography (PET) and the radiotracer [(18)F]setoperone.

Propofol reduces cognitive impairment after electroconvulsive therapy.

Background: Cognitive impairments are the main complication after electroconvulsive therapy (ECT). Modification of treatment parameters has been shown to affect the magnitude of these impairments, but the role of anesthetic type remains unclear. This study tested whether there is a difference in cognitive impairments immediately after ECT with propofol compared to thiopental anesthesia.

Repeated electroconvulsive shock attenuates the depressive-like effects of d-amphetamine withdrawal on brain reward function in rats.

Rationale: The withdrawal of humans from high doses of psychostimulant drugs can result in a transient syndrome which appears isomorphic to endogenous depression. One of the more prominent symptoms is a loss of hedonic capacity; in animals, the anhedonia associated with amphetamine withdrawal has been measured objectively by decrements in responding for intracranial self-stimulation (ICSS).

Objective: To date, the effects of amphetamine withdrawal on ICSS responding have been reversed by different antidepressant drugs.

Effect of Stimulus Energy on Electroconvulsive Therapy-Induced Prolactin Release.

This study was undertaken to examine the effect of stimulus energy on electroconvulsive therapy (ECT)-induced prolactin (PRL) release. Patients undergoing a course of right unilateral or bilateral ECT were studied during two consecutive treatments. The order of high- and low-energy ECT was counterbalanced between the two treatments.

The Role of Dopamine in Seizure-Induced Prolactin Release in Humans.

Prolactin (PRL) plasma levels rise severalfold following spontaneous or electrically induced seizures. To assess the role of dopamine in this neuroendocrine response, we studied the effect of electroconvulsive therapy (ECT) on plasma PRL after maximal dopamine receptor blockade induced by intravenous metoclopramide. Six patients undergoing ECT received metoclopramide or placebo, in counterbalanced order, 30 min prior to application of the electrical stimulus.