The effect of acute and repeated electroconvulsive treatment on plasma β-endorphin, growth hormone, prolactin and cortisol secretion in depressed patients

Weizman, Abraham; Gil-Ad, Irit; Grupper, Daniel; Tyano, Sam; Laron, Zvi

doi:10.1007/bf02439598

Cited by 51 publications

(35 citation statements)

References 37 publications

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“…Baseline cortisol levels were 30% greater in patients than in controls, but there were no differences from baseline levels after ECT sessions are consistent with the findings reported by Aperia et al, 16 Aperia et al, 20 Weizman et al 23 and Ozsoy et al 40 Ozsoy et al 40 suggested that the mechanism of action of ECT might be explained by the fact that it changes the instability of levels of neuroactive steroids that affect gamma-aminobutyric acid (GABA)…”

Section: Discussionsupporting

confidence: 81%

Variation of plasma cortisol levels in patients with depression after treatment with bilateral electroconvulsive therapy

Burgese

Bassitt

2015

Trends Psychiatry Psychother.

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Introduction: More than 60 years after the introduction of modern psychopharmacology, electroconvulsive therapy (ECT) continues to be an essential therapeutic modality in the treatment of mental disorders, but its mechanism of action remains unclear. Hormones play an essential role in the development and expression of a series of behavioral changes. One aspect of the influence of hormones on behavior is their potential contribution to the pathophysiology of psychiatric disorders and the mechanism of action of psychotropic drugs and ECT. Objective: We measured blood levels of the hormone cortisol in patients with unipolar depression according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) and compared results with levels found in healthy adults. Method: Blood cortisol levels were measured before the beginning of treatment with ECT, at the seventh session, and at the last session, at treatment completion. Depression symptoms were assessed using the Beck Depression Inventory (BDI). Results: Cortisol levels remained stable in both men and women between the seventh and the last sessions of ECT; values ranged from 0.686±9.6330 g/dL for women, and there was a mean decrease of 5.825±6.0780 g/dL (p = 0.024). Mean number of ECT sessions was 12. After the seventh and the last ECT sessions, patients with depression and individuals in the control group had similar cortisol levels, whereas BDI scores remained different. Conclusion: Cortisol levels decreased during ECT treatment. ECT seems to act as a regulator of the hypothalamic-pituitaryadrenal axis.

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Section: Discussionsupporting

confidence: 81%

Variation of plasma cortisol levels in patients with depression after treatment with bilateral electroconvulsive therapy

Burgese

Bassitt

2015

Trends Psychiatry Psychother.

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“…The neuropeptide hypothesis suggests that dysregulation of hypothalamic peptides underlies the pathogenesis of affective disorders (4,25,(35)(36)(37). In depressed patients who respond to a course of ECS treatment, ECS alters neuroendocrine secretion of CRH, fi-endorphin, growth hormone, prolactin, and somatostatin (36,(38)(39)(40)(41). Our findings suggest a merger of the two hypotheses: the antidepressant effects of ECS are mediated by an initial activation of neurotransmitter systems including the LC-NE system followed by a delayed activation of hypothalamic neuropeptide systems, primarily CRH.…”

Section: Discussionmentioning

confidence: 99%

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Brady

Lynn²,

Glowa³

et al. 1994

J. Clin. Invest.

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Electroconvulsive shock (ECS) is a highly effective therapy for the treatment of major depression, but its mechanisms of action are not known. We report that repeated ECS in rats produces enduring changes in two clinically relevant stress-responsive brain systems: (a) the hypothalamic-pituitary-adrenal axis regulated by corticotropin-releasing hormone (CRH) in the paraventricular nucleus; and (b) the NE system in the locus coeruleus regulated by tyrosine hydroxylase (TH). CRH and TH mRNA levels in these brain regions were assessed by in situ hybridization histochemistry. A single interaural ECS elevated TH but not CRH mRNA measured 24 h later. Repeated daily treatments (3, 7, or 14) elevated both mRNAs, maximally with 7, correlating with the time course of clinical efficacy. The elevations persisted for 3 (CRH) or 8 wk (TH) after the ECS. No other therapeutic treatment is known to produce such longlasting changes in central nervous system gene expression. The time course of events (delayed onset, long duration) implicate CRH as a principal mediator of the antidepressant effects of ECS. The locus coeruleus-NE system may be important in initiating the central nervous system response. (J. Clin. Invest. 1994.94:1263-1268

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“…Beneficial effects of electroconvulsive treatment is associated with elevations of plasma beta endorphine level in depressed patients [21,22].…”

Section: Antidepressant Effects Of Endorphin Agonists: Animal and CLImentioning

confidence: 99%

Endorphin agonists for psychiatric disorders

Salerian¹

2016

Phys Med Rehabil Res

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Endorphins and endorphin agonists play a crucial role in the neural modulation of mood, anxiety, pain and addiction.Historical, experimental and clinical data strongly support the potential benefits of opiates for severe depression, addictive disorders, pain and psychosis. Recent studies have also elucidated a crucial mechanism of treating depression-enhancing prefrontal cortex influence and dampening limbic and sub cortical influencessimilar to the neurobiological actions of endorphin agonists.Despite much publicity of an alleged causal association between prescription pain medications and an epidemic of overdose deaths, no scientific evidence exists to support a causal link between prescription opiates and the overdose deaths.Despite concerns of addiction and misuse potential further research to study endorphin agonists for diverse psychiatric disorders seems warranted.Correspondence to: Alen J Salerian, Salerian Center for neuroscience and pain, 8409 Carlynn Dr.,

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The effect of acute and repeated electroconvulsive treatment on plasma β-endorphin, growth hormone, prolactin and cortisol secretion in depressed patients

Cited by 51 publications

References 37 publications

Variation of plasma cortisol levels in patients with depression after treatment with bilateral electroconvulsive therapy

Variation of plasma cortisol levels in patients with depression after treatment with bilateral electroconvulsive therapy

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Endorphin agonists for psychiatric disorders

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