N alpha-acetyl-beta-endorphin stimulates ornithine decarboxylase activity in preweanling rat pups: opioid- and non-opioid-mediated mechanisms.

Our laboratory has demonstrated recently that administration of beta-endorphin to rat pups results in profound changes in the levels of the growth-related enzyme ornithine decarboxylase (ODC) in both brain and peripheral tissues. These findings are consistent with accumulated evidence indicating that, in addition to their analgesic and behavioral effects in the adult, endogenous opioid peptides and opioid receptors may be involved as mediators of tissue growth and function in the neonate. This study examines the effects of N alpha-acetyl-beta-endorphin on tissue ODC activity to determine whether post-translational acetylation of beta-endorphin at the N alpha-terminus affects its capability to alter ODC activity and, consequently, tissue development. Intracisternal administration of N alpha-acetyl-beta-endorphin evoked profound increases in brain ODC activity in 6- and 9-day-old rats, whereas normal ODC levels were observed in 25-day-old animals and in adult rats. Centrally administered N alpha-acetyl-beta-endorphin had no effect on ODC in peripheral tissues. In contrast, s.c. administration of this peptide to 6-day-old animals resulted in marked increases in ODC activity in the heart, liver and brain. Naloxone inhibited the stimulatory actions of N alpha-acetyl-beta-endorphin on brain ODC completely, indicating the involvement of opioid receptors in that process. On the other hand, the increases in liver ODC were not prevented by naloxone, suggesting that these effects are not mediated through opioid-sensitive structures.(ABSTRACT TRUNCATED AT 250 WORDS)