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Long‐Term Treatment of Rats with Morphine Reduces the Activity of Messenger Ribonucleic Acid Coding for the β‐Endorphin/ACTH Precursor in the Intermediate Pituitary
Author(s) -
Höllt Volker,
Haarmann Ingeborg,
Herz Albert
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb12532.x
Subject(s) - medicine , endocrinology , endorphins , reticulocyte , morphine , messenger rna , anterior pituitary , phenylalanine , chemistry , hypothalamus , pituitary gland , beta endorphin , in vitro , proopiomelanocortin , posterior pituitary , opiate , prohormone , peptide hormone , biology , amino acid , biochemistry , hormone , receptor , gene
Chronic administration of morphine to rats for a period of 4 weeks resulted in a 50‐60% decrease in the tissue concentrations of β‐endorphin and in the in vitro release from the neurointermediate pituitary. Incorporation of [ 3 H]phenylalanine into isolated intermediate/posterior pituitaries in vitro revealed a reduction in the amount of label incorporated into the β‐endorphin/ ACTH precursor to a similar extent (about 45%), but essentially no effect on the conversion of the precursor into β‐lipotropin and β‐endorphin. Extraction of mRNA from intermediate/posterior pituitaries followed by cell‐free translation in a reticulocyte system showed no significant decrease in the total level of translatable mRNA. In contrast, the content of translatable mRNA coding for the β‐endorphin/ACTH precursor was significantly reduced by 50‐60%. Thus, long‐term treatment with morphine appears to depress β‐endorphin formation in the rat intermediate pituitary at the pretranslational level by markedly decreasing the activity of mRNA coding for the β‐endorphin/ACTH precursor without any alteration in the processing of this precursor.