Benzodiazepine suppression of corticotropin-releasing factor (CRF)-induced beta-endorphin release from rat neurointermediate pituitary

L. C. Saland, J. A. Carr, A. Samora, D. Tejeda

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Dopamine and gamma-aminobutyric acid (GABA) inhibit POMC peptide release from the pituitary intermediate lobe, via interaction with D2 or GABA-A/benzodiazepine receptors. Here, we examined the effects of an antianxiety triazolobenzodiazepine, adinazolam, on corticotropin-releasing factor (CRF)-stimulated POMC peptide secretion from the rat neurointermediate pituitary. Neurointermediate lobes (NILS) were incubated with CRF (10-7 M), then adinazolam (10-8 or 10-9 M) was added, with CRF remaining in the medium. Aliquots were removed at 15-min intervals and frozen for radioimmunoassay of beta-endorphin. Adinazolam alone did not significantly affect secretion as compared to controls or CRF alone. Adinazolam incubated with CRF led to significant inhibition of beta-endorphin secretion, as compared to CRF alone. In addition, adinazolam was as effective as dopamine or the CRF antagonist, alpha-helical CRF, in preventing CRF-induced beta-endorphin release. Adinazolam appears to act directly on the pituitary to suppress hormone release induced by a stress-related hypothalamic peptide.

Original languageEnglish
Pages (from-to)913-917
Number of pages5
JournalPeptides
Volume13
Issue number5
DOIs
StatePublished - 1992

Keywords

  • Adinazolam
  • Benzodiazepines
  • Beta-endorphin
  • CRF
  • Pituitary gland
  • Rats

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