Abstract
Glucocorticoids regulate sympathoadrenal catecholamine (CA) biosynthesis. We determined whether co-localized adrenal opiate peptides are also subject to hormonal control. Adrenal cortical destruction (mitotane) decreased baseline leuenkephalin (LEU) levels in vivo by 38% (p<0.05). To examine cellular mechanisms, rat medullae were grown as explants in glucocorticoid deficient medium. LEU levels start low then increase in a dose-dependent fashion following corticosterone replacement (zero to 10−5 M) .Effects of glucocorticoids could be blocked by alkylating (CM-21, DM-21) or non-alkylating (cortexolone) receptor antagonists added to corticosterene containing medium. Moreover, inhibition of glucocorticoid receptor translocation to the nucleus ( cytochalasin B) also blocked the hormone effect. In addition, a 13 out of 17 nucleic acid match for a putative glucocorticoid receptor binding site was identified in intron A of the rat preproenkephalin genome. These observations are consistent with dual hormonal, and transsynaptic regulation (La Gamma, et al PNAS 82:8252, 1985) of opiate biosynthetic processes. Therefore, similar to CA, LEU exhibits significant transmitter plasticity which may serve an adaptive role in modulating complex biochemical and behavioral responses (eg. during stress or development) with exquisite precision. Supported in part by the American Heart Association.
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La Gamma, E., Adler, J. & Black, I. GLUCOCORTICOIDS REGULATE ADRENAL OPIATE PEPTIDES. Pediatr Res 21 (Suppl 4), 248 (1987). https://doi.org/10.1203/00006450-198704010-00488
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DOI: https://doi.org/10.1203/00006450-198704010-00488