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Naloxone has no effect on hormonal responses to ECT in man
1Department of Psychological Medicine, St. Bartholomew's Hospital, West Smithfield, London.
Psychiatry Research
|November 1, 1987
Summary
Electroconvulsive therapy (ECT) increases serum prolactin in humans, but this effect is not due to endogenous opioids. This study found that naloxone, an opiate antagonist, did not alter ECT-induced prolactin release.
Area of Science:
- Neuroendocrinology
- Psychopharmacology
Background:
- Electroconvulsive therapy (ECT) is known to alter endogenous opioid activity in animal models.
- Limited human data exist regarding the role of endogenous opioids in ECT's neuroendocrine effects.
- ECT-induced changes in hormones like serum prolactin suggest a potential link to opioid pathways.
Purpose of the Study:
- To investigate the involvement of endogenous opioid peptides in the human prolactin response to electroconvulsive therapy (ECT).
- To determine if the opiate antagonist naloxone modulates ECT-induced changes in serum prolactin, growth hormone (GH), and cortisol.
Main Methods:
- A double-blind, randomized crossover study involving six unmedicated major depressive illness patients.
- Administration of intravenous naloxone or saline control before successive ECT treatments.
- Serial blood sampling to measure serum prolactin, GH, and cortisol levels post-ECT.
Main Results:
- Electroconvulsive therapy (ECT) significantly increased serum prolactin levels.
- No significant changes were observed in serum growth hormone (GH) or cortisol levels within the 20-minute sampling interval.
- Naloxone administration did not significantly affect the ECT-induced rise in serum prolactin or other measured hormones.
Conclusions:
- The observed increase in serum prolactin following electroconvulsive therapy (ECT) in humans is not mediated by endogenous opioid peptide activity.
- These findings suggest that other neuroendocrine mechanisms are responsible for the prolactin response to ECT.