60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-prolactin axis

  1. David R Grattan1,2
  1. 1Centre for Neuroendocrinology and Department of Anatomy, University of Otago, PO Box 913, Dunedin 9054, New Zealand
    2Maurice Wilkins Centre for Molecular Biodiscovery, Auckland, New Zealand
  1. Correspondence should be addressed to D R Grattan; Email: dave.grattan{at}otago.ac.nz
  1. Figure 1

    Diagrammatic representation of the neuroendocrine regulation of prolactin secretion. Anterior pituitary prolactin release is inhibited by dopamine coming from the tuberoinfundibular dopamine neurons (shown in the coronal section on the top left using immunohistochemistry against tyrosine hydroxylase, brown) whose cell bodies are found in the arcuate nucleus of the hypothalamus, with axons projecting to the external layer of the median eminence. Images on the right show examples of both rapid feedback (electrophysiological activation) and delayed feedback (phosphorylation of STAT5, black nuclear staining) in TIDA neurons. In each example, 1) illustrates prior to prolactin treatment, and 2) after administration of prolactin (reproduced, with permission, from Brown RS, Piet R, Herbison AE & Grattan DR (2012) Differential actions of prolactin on electrical activity and intracellular signal transduction in hypothalamic neurons. Endocrinology 153 2375–2384. Copyright 2012 The Endocrine Society). Prolactin stimulates dopamine secretion, to inhibit its own secretion by short loop feedback.

  2. Figure 2

    (A) Diagrammatic representation of short loop feedback control of prolactin secretion. (B) Adaptive changes in the regulation of prolactin secretion during pregnancy and lactation. Note that there are multiple adaptive processes to ensure elevated levels of lactogenic hormones present both in the blood and in the brain of the mother, potentially regulating a wide range of functions to facilitate lactation: 1) Production of prolactin-like molecules from the placenta to bypass feedback regulation of pituitary prolactin secretion. 2) Plasticity in the TIDA neuronal response to prolactin, with reduced secretion of dopamine and induction of enkephalin expression. 3) Maternal behavioural adaptation to suckle the pups, providing the most powerful prolactin-releasing stimulus known. 4) Increased transport of prolactin into the brain during lactation.

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  1. J Endocrinol 226 T101-T122
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