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  • Title: The rat posterior pituitary contains a potent prolactin-releasing factor: studies with perifused anterior pituitary cells.
    Author: Hyde JF, Murai I, Ben-Jonathan N.
    Journal: Endocrinology; 1987 Oct; 121(4):1531-9. PubMed ID: 2888647.
    Abstract:
    UNLABELLED: We previously reported that removal of the posterior pituitary abolished the suckling-induced rise in plasma PRL. This suggested that the posterior pituitary contains a PRL-releasing factor (PRF). Using perifused anterior pituitary cells, the objectives of this study were 1) to examine whether the posterior pituitary contains PRF activity as compared to the medial basal hypothalamus (MBH), and 2) to determine to what extent substances known to be present in the posterior pituitary and/or MBH contribute to this activity. Anterior pituitary cells, attached to Cytodex beads, were perifused with medium 199. Tissues were extracted with acid, lyophilized, and reconstituted in medium 199. Tissue extracts and synthetic compounds were introduced to the cells in short pulses. Fractions were collected and analyzed for PRL, LH, and GH by RIA. Posterior pituitary extracts contained a potent substance(s) which stimulated PRL release in a concentration-dependent manner, but did not alter LH secretion. As little as 1% of the extract increased PRL release. In contrast, the MBH extract contained significantly less PRF activity but was capable of stimulating and inhibiting LH and GH release, respectively. Cerebellar extracts did not alter PRL secretion. Of more than 25 neuroactive substances tested in the perifusion system, oxytocin, TRH, and angiotensin II (A II) appeared as likely candidates for PRF. Therefore, the specific receptor antagonists d(CH2)5Tyr(Me) ornithine vasotocin (for oxytocin), chlordiazepoxide (for TRH), or saralasin (for A II) were infused together with the posterior pituitary extract. These antagonists completely abolished the PRL-releasing activities of their respective peptides but failed to reduce the PRF activity of the posterior pituitary. In contrast, PRF activity in the MBH was nearly eliminated by the TRH antagonist. CONCLUSIONS: 1) The rat posterior pituitary contains a potent PRF capable of inducing a rapid, hormone-specific, concentration-dependent stimulation of PRL release from perifused anterior pituitary cells. 2) The MBH contains significantly less PRF activity, which is largely attributable to TRH. 3) Although the chemical identity of PRF is yet unknown, the PRF activity in the posterior pituitary is not accounted for by oxytocin, TRH, or A II.
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