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Abstract:
Samples of 1 microliter containing 15 microgram of morphine sulfate with or without 1 microgram of synthetic ACTH were injected into the fourth ventricle of rats. The inclusion of ACTH eliminated the analgesic effect of morphine as evaluated by the tail-flick test, both in restrained and in unrestrained, lightly sedated animals. The same result was obtained when beta-endorphin was used to bring about analgesia. Since the effect of the peptides was shown to be mediated by central actions alone, the results are discussed in light of the brain ACTH/beta-endorphin system.
Insights
Adrenocorticotropic hormone (ACTH) blocks the pain-relieving effects of morphine and beta-endorphin in rats. This suggests the brain
Area of Science:
- Neuroscience
- Pharmacology
- Endocrinology
Background:
- Morphine and beta-endorphin are known analgesics.
- Adrenocorticotropic hormone (ACTH) plays a role in the stress response.
- The interaction between opioid and ACTH systems in the brain is not fully understood.
Purpose of the Study:
- To investigate the effect of synthetic ACTH on morphine-induced analgesia in rats.
- To determine if ACTH modulates the analgesic effects of beta-endorphin.
- To explore the role of the central ACTH/beta-endorphin system in pain modulation.
Main Methods:
- Rats received injections of morphine sulfate and/or synthetic ACTH into the fourth ventricle.
- Analgesia was assessed using the tail-flick test in both restrained and unrestrained conditions.
- Beta-endorphin was used as an alternative analgesic agent to test ACTH's effect.
Main Results:
- The presence of synthetic ACTH completely abolished the analgesic effect of morphine sulfate.
- ACTH also eliminated the analgesia produced by beta-endorphin.
- These effects were observed regardless of whether the rats were restrained or unrestrained.
Conclusions:
- Central ACTH administration antagonizes the analgesic properties of both morphine and beta-endorphin.
- The findings highlight the significant role of the brain's ACTH/beta-endorphin system in pain perception.
- This interaction suggests a complex interplay between the endocrine and central nervous systems in pain regulation.