Studies of the neural mechanisms by which hypothyroidism decreases prolactin secretion in the rat

Gloria Jahnke, Gayle Nicholson, G. H. Greeley, W. W. Youngblood, A. J. Prange, J. S. Kizer

    Research output: Contribution to journalArticlepeer-review

    26 Scopus citations

    Abstract

    These studies report that chronic hypothyroidism in the rat is accompanied by decreased serum prolactin. An investigation of those mechanisms by which hypothyroidism decreases prolactin secretion revealed the following findings: 1. (1) activation of tyrosine hydroxylase in the median eminence (ME) and increase in the turnover-rate of dopamine (DA) in the ME; 2. (2) a decreased content and in vitro release of prolactin by pituitaries from hypothyroid rats; 3. (3) decreased [3H]spiroperidol binding to pituitary homogenates obtained from hypothyroid rats, and 4. (4) normal increase of serum prolactin following administration of haloperidol. Comparison of the effects of hypothyroidism on dopaminergic terminals of the striatum with those of the ME was made and the following tentative conclusions proposed. Hypothyroidism presumably increases the release of DA into the pituitary portal system. A deficiency of thyroid hormone desensitizes the pituitary lactrotrope to inhibition by DA, decreases the total pituitary prolactin content and presumably also reduces the peripheral catabolism of prolactin. The overall net effect of hypothyroidism is therefore, a decrease in serum prolactin levels which can increase normally following haloperidol. The mechanism by which a deficiency of thyroid hormone alters the function of the tuberoinfundibular and striatal dopaminergic systems is unknown.

    Original languageEnglish (US)
    Pages (from-to)429-441
    Number of pages13
    JournalBrain Research
    Volume191
    Issue number2
    DOIs
    StatePublished - Jun 9 1980

    Keywords

    • haloperidol
    • hypothalamus
    • hypothyroidism
    • prolactin
    • [H]spiroperidol

    ASJC Scopus subject areas

    • Developmental Biology
    • Molecular Biology
    • Clinical Neurology
    • Neuroscience(all)

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