Neuroendocrine Study of the Mechanism of Action of Electroconvulsive Therapy

Arató, M.; Bagdy, György

doi:10.1159/000117894

Cited by 11 publications

(4 citation statements)

References 13 publications

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“…Plasma levels of prolactin (PRL) increase after the administration of electroeonvulsive therapy (ECT) (Ohman et al 1976;O'Dea et al 1978;Skrabanek et al 1981;Arato and Bagdy 1982;Balldin 1982;Whalley et al 1982). Several observations suggest that this PRL release is the result of the generalized seizure.…”

Section: Introductionmentioning

confidence: 99%

Hormone response to repeated electroconvulsive therapy: Effects of naloxone

Haskett

Zis

Albala

1985

Biological Psychiatry

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Plasma prolactin (PRL), cortisol, and growth hormone (GH) were measured before, and at 15-min intervals for 1 hr after, electroconvulsive therapy (ECT). This was repeated over a series of 6 consecutive treatments for each of 12 depressed drug-free inpatients. Patients received naloxone, 2 mg or 20 mg, by intravenous infusion before the third and fifth treatment. ECT was consistently followed by a release of PRL and cortisol, although two patterns of PRL response could be distinguished. In eight patients, the PRL response did not change significantly with repeated ECT, whereas in four patients, the plasma PRL increased tenfold after the first treatment and decreased after each successive treatment. The GH level varied widely, with no evidence of a reliable response to ECT. Opiate receptor blockade with low- or high-dose naloxone did not alter the release of PRL or cortisol after ECT. These findings demonstrate a reliable PRL and cortisol response to ECT, but do not support a role for endogenous opiates in these hormonal changes.

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Section: Introductionmentioning

confidence: 99%

Hormone response to repeated electroconvulsive therapy: Effects of naloxone

Haskett

Zis

Albala

1985

Biological Psychiatry

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“…Naloxone treatment was effective in some manic patients (Janowsky 1978) while fl-endorphin (fl-EP) treatment was beneficial in some depressed patients (Kline et al 1979). ECT administration to depressed patients induces changes in fl-EP (Emrich et al 1979;Alexopoulos et al 1983;Misiaszek et al 1984), growth hormone (GH), prolactin (Prl) and cortisol levels (O'Dea et al 1978;Skrabanek et al 1981 ;Arato 1982;Balldin 1982;Whalley et al 1982;Deakin et al 1983;Linnoila et al 1984;Swartz and Abrams 1984). The hormonal effects might be attributed to the ECT impact on neurotransmitters or on neuromodulators or to a non-specific stress effect which stimulates the hypothalamic-pituitary-adrenal (HPA) axis.…”

mentioning

confidence: 99%

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

et al. 1987

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The effects of single and repeated electroconvulsive treatment (ECT) on beta-endorphin (beta-EP), cortisol, growth hormone (GH) and prolactin (Prl) plasma levels were investigated in nine depressed patients. Blood samples were monitored a day before ECT, the day of the first and sixth ECT (0, 30, 60 and 90 min after seizures), the day afterwards and 4 weeks after termination of the ECT course. A significant elevation of beta-EP levels was achieved immediately with and 24 h after the first and the sixth ECT. A transient increase in basal beta-EP was observed 1 day following the sixth ECT in comparison with pre-treatment level. Peak and 30 min levels of cortisol were increased compared with baseline by the first ECT. The former (peak) but not the latter (30 min) were increased also at the sixth treatment. GH levels were decreased the day after the first ECT in comparison with the pre-treatment levels and immediately following each ECT in comparison with baseline. A trend toward elevation of Prl was observed immediately after the first and sixth ECT, although the rise did not reach significant levels. ECT administration stimulated beta-EP and cortisol secretion and suppressed human GH release, possibly by activation of endorphinergic and/or serotonergic systems. These mechanisms might be involved in the beneficial effect of ECT in depression.

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“…Those monoamines which have been implicated in the regulation of pubertal onset (Advis, Simpkins, Chen & Meites, 1978;Wuttke, Honma, Lamberts & Höhn, 1980), may also be responsible for mediating the antidepressant effect of ECS (Grahame-Smith, Green & Costain, 1978;Green & Deakin, 1980), and it has been demonstrated that repeated ECS decreases ct2-adrenoceptor density in the hypothalamus (Stanford & Nutt, 1982). These data, together with evidence of altered prolactin secretion following ECS in rats (Bhanot & Wilkinson, 1984) and man (Arato & Bagdy, 1982;Whalley, Dick, Watts et al 1982) strongly suggest that the hypothalamic monoaminergic system is disrupted and hence inter¬ ference in reproductive hormone secretion is involved in the ECS-induced delay in puberty. However, electroconvulsions are also associated with a plethora of neurochemical changes, and the possibility of a role for other systems, such as the EOP, in the efficacy of this effect cannot be excluded.…”

Section: Discussionmentioning

confidence: 96%

Seizure-induced delay of puberty in female rats: effects of age, stress and opioid antagonists

Carson

Wilkinson²

1989

Journal of Endocrinology

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We have shown that pre- and post-pubertal female rats are sensitive to seizures. For example, daily convulsions commencing at 24 days of age delay puberty. Here we examine the effect of seizures at various ages. In addition, because opioid peptides are implicated in regulating the onset of puberty and are activated by convulsions, we also investigate the effect of opioid antagonists in the seizure-induced delay of puberty. A single daily electroconvulsive shock (ECS) was given for 10 days to neonatal (days 2-11), infantile (days 15-24) and juvenile (days 22-31) rats. The treatment delayed vaginal opening (VO) in juvenile rats. Neonatal and infantile rats were unaffected. VO was also delayed by daily ECS for only 5 days in the late juvenile (days 27-31) period. The opioid receptor antagonists naloxone, naltrexone and nalmefene injected before and after single daily ECS were unable to block this effect of ECS on VO. To examine whether the effect of ECS is related to stress, we examined several stressors known to induce opioid-mediated alterations in gonadotrophin secretion. Footshock, immobilization and ether stress administered in the juvenile period (days 27-31) did not affect the timing of VO. In addition, rats anaesthetized with halothane, and then given ECS, still showed a delay of VO. These data demonstrate that rats in the late juvenile stage of development are most sensitive to convulsions. We also suggest that opioids are not critical to the mechanism by which the ECS disturbs puberty, and that ECS elicits its effect seemingly independently of the convulsive stress.

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Neuroendocrine Study of the Mechanism of Action of Electroconvulsive Therapy

Cited by 11 publications

References 13 publications

Hormone response to repeated electroconvulsive therapy: Effects of naloxone

Hormone response to repeated electroconvulsive therapy: Effects of naloxone

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

Seizure-induced delay of puberty in female rats: effects of age, stress and opioid antagonists

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