The role of pituitary β-endorphin in mediating corticotropin-releasing factor-induced antinociception

K. M. Hargreaves, C. M. Flores, R. A. Dionne, G. P. Mueller

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

The hypothesis that blood-borne β-endorphin modulates nociception was examined with corticotropin-releasing factor (CRF) as a potent and selective agent to stimulate its release from the pituitary gland. Intravenously administered CRF produced a dose-related antinociception in rats as determined by measuring paw-lick latencies on a 50°C hot plate. A dose of 25 nmol/kg of CRF was comparable in both magnitude and duration of antinociception to a 7,500 nmol/kg (= 2.5 mg/kg) dose of morphine sulfate. The antinociceptive effect of CRF was blocked by both hypophysectomy and dexamethasone pretreatment, suggesting that it was mediated by hormone release from the anterior pituitary corticotrophs. Furthermore, the effect of CRF was antagonzied by 1) naltrexone, 2) naltrexone methyl bromide, and 3) passive immunization with anti-β-endorphin antiserum. Together, these data support the hypothesis that opiate-active, β-endorphin, released by pituitary corticotrophs, participates in the physiological modulation of nociception in rats.

Original languageEnglish (US)
Pages (from-to)E235-E242
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume258
Issue number2 21-2
StatePublished - Jan 1 1990
Externally publishedYes

Keywords

  • analgesia
  • beta-endorphin
  • corticotropin-releasing factor
  • pain
  • pituitary

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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