Altered Ratios of Beta-Endorphin:Beta-Lipotropin Released from Anterior Lobe Corticotropes with Increased Secretory Drive.

Abstract

A number of stimuli including acute footshock and electrically-induced seizures lead to release of Β-endorphin immunoreactivity from the anterior pituitary corticotropes. Gel filtration of this Β-endorphin immunoreactivity indicates that approximately 3-fold more Β-endorphin than Β-lipotropin is released into plasma following these acute stressors. A similar preponderance of Β-endorphin over Β-lipotropin is seen in the media of short-term anterior lobe cell suspensions stimulated with ovine corticotropin-releasing hormone. Previous studies indicated that footshock stress, when administered repeatedly, can increase the biosynthesis of anterior lobe proopiomelanocortin (POMC) as indicated by increased steady state adrenocorticotropin/Β-endorphin content as well as increased POMC mRNA levels and increased POMC biosynthesis and rate of processing as measured by pulse-labeling and pulse-chase studies. The goal of the present studies was to determine whether this increased biosynthetic drive results in an alteration in the end products secreted with repeated stress. Acute footshock in a rat which has received 14 days of chronic footshock releases proportionately more Β-lipotropin than is released in a naive rat. Chronic electrically-induced seizures, which also increase anterior lobe POMC derived peptide stores, lead to a similar shift in the ratio of Β-lipotropin:Β-endorphin released following stress. These data suggest that chronic drive and the subsequent changes in POMC peptide stores may lead to a decrease in the proportion of Β-endorphin size immunoreactivity in the releasable pool of the anterior lobe corticotrope, thus altering the hormonal signal from the anterior lobe corticotrope.