Effect of protein synthesis inhibition on brain corticotropin-releasing factor and plasma adrenocorticotropin.
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.
Haas
D A
DA
Department of Medicine, University of Toronto, Ont., Canada.
Sturtridge
W C
WC
George
S R
SR
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D001923:Brain Chemistry / Q000187:drug effects*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008473:Median Eminence / Q000187:drug effects / Q000378:metabolism; D014176:Protein Biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains
D000841:Anisomycin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone