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Title page for ETD etd-07132009-125545


Type of Document Dissertation
Author McKee, De'Nise
Author's Email Address mckee@neuro.fsu.edu
URN etd-07132009-125545
Title Control of Prolactin Secretion by Central Oxytocin in Cervically Stimulated Ovariectomized Rats
Degree Doctor of Philosophy
Department Biological Science, Department of
Advisory Committee
Advisor Name Title
J Michael Overton Committee Member
Michael Meredith Committee Member
Richard Bertram Committee Member
Timothy Logan Outside Committee Member
Keywords
  • Prolactin
  • Oxytocin
  • Neuroendocrinology
  • Hypothalamus
Date of Defense 2009-07-09
Availability unrestricted
Abstract
Prolactin is a protein hormone predominately synthesized in and secreted from cells in the anterior pituitary gland called lactotrophs. Although prolactin is elevated during other physiological states, mating induces a unique pattern of prolactin secretion. Prolactin is elevated twice a day for several days in response to a mating stimulus, suggesting a mnemonic. The neural pathway in which the mating stimulus initiates this unique prolactin secretion is unknown. However, hypothalamic inhibitory neuroendocrine dopamine neurons and stimulatory oxytocin neurons are demonstrated to be involved. Our laboratory has shown that a peripheral injection of oxytocin initiates prolactin surges like those induced by mating. This suggests that oxytocin may initiate the mating-induced prolactin surges. Whether the bolus injection of oxytocin initiated these surges by acting peripherally or centrally was investigated in this dissertation. Results showed that oxytocin does not initiate these surges by acting peripherally since a peripheral oxytocin antagonist did not block the initiation of the surges. However, peripheral oxytocin is important for maintaining the surges. Therefore, central oxytocin must initiate twice daily prolactin surges, likely from the hypothalamic paraventricular nucleus. Since the mating stimulus must convey its signal from the uterine cervix to the hypothalamus a pathway was investigated. A relay of the mating stimulus via brainstem noradrenergic input to the paraventricular nucleus was shown. Only brainstem noradrenergic neurons that projected to paraventricular nucleus were activated by the mating stimulus, suggesting a specific pathway for the initiation of mating-induced prolactin surges. In addition, norepinephrine was released in the paraventricular nucleus in response to a mating stimulus. Lastly, oxytocin neurons in the hypothalamic paraventricular nucleus were directly investigated. Surprisingly, hypothalamic oxytocin neurons were not acutely activated by a mating stimulus, suggesting that the paraventricular nucleus is not a source of oxytocin important in initiating the mating-induced prolactin surges.
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