Effect of protein synthesis inhibition on brain corticotropin-releasing factor and plasma adrenocorticotropin

Can J Physiol Pharmacol. 1990 Dec;68(12):1595-600. doi: 10.1139/y90-243.

Abstract

The effect of inhibiting protein synthesis on concentrations of corticotropin-releasing factor (CRF) in rat brain and plasma adrenocorticotropin (ACTH) was assessed following the administration of the general protein synthesis inhibitor anisomycin. Compared with vehicle-injected controls, protein synthesis inhibition resulted in significantly reduced CRF immunoreactivity (CRF-ir) in median eminence within 1 h (p less than 0.01), remained decreased after 4 h (p less than 0.025), and was nonsignificantly decreased after 24 h. Plasma ACTH levels were greatly increased within 1 h posttreatment (p less than 0.0005), continued elevated after 4 h (p less than 0.01), and returned to normal levels after 24 h. CRF-ir measured in other brain areas 24 h after anisomycin showed decreased levels in medulla-pons (p less than 0.025) and neurointermediate lobe of pituitary (p less than 0.05), with no change noted in frontal cortex, hippocampus, midbrain-thalamus, or cerebellum. Overall these data show that blockade of normal protein synthesis with anisomycin can elicit changes in CRF-ir and ACTH content.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenocorticotropic Hormone / blood*
  • Animals
  • Anisomycin / pharmacology
  • Brain Chemistry / drug effects*
  • Corticotropin-Releasing Hormone / metabolism*
  • Hypothalamus / drug effects
  • Hypothalamus / metabolism
  • Male
  • Median Eminence / drug effects
  • Median Eminence / metabolism
  • Protein Biosynthesis*
  • Rats
  • Rats, Inbred Strains

Substances

  • Anisomycin
  • Adrenocorticotropic Hormone
  • Corticotropin-Releasing Hormone