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Stress-induced release of prolactin - blockade by dexamethasone and naloxone may indicate beta-endorphin mediation

Academic Article
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Overview

authors

  • Rossier, J.
  • French, E.
  • Rivier, Catherine
  • Shibasaki, T.
  • Guillemin, R.
  • Bloom, Floyd

publication date

  • 1980

journal

  • Proceedings of the National Academy of Sciences of the United States of America-Biological Sciences  Journal

abstract

  • Basal levels of immunoreactive (ir) beta-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 microgram/kg at 24 hr and 200 microgram/kg at 2 hr before). Inescapable electric footshocks increase ir-beta-endorphin, ACTH, and PRL plasma levels and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-beta-endorphin, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-beta-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir-beta-endorphin. These results are consistent with the proposal that beta-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.

subject areas

  • Adrenocorticotropic Hormone
  • Animals
  • Dexamethasone
  • Endorphins
  • Morphine
  • Naloxone
  • Pituitary Gland
  • Prolactin
  • Rats
  • Secretory Rate
  • Stress, Physiological
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Identity

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.77.1.666

PubMed ID

  • 6244573
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Additional Document Info

start page

  • 666

end page

  • 669

volume

  • 77

issue

  • 1

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