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      Progesterone Reverses the Estradiol-lnduced Decrease in Tyrosine Hydroxylase mRNA Levels in the Arcuate Nucleus

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          Estradiol (E<sub>2</sub>) and progesterone (P<sub>4</sub>) interact to influence tuberoinfundibular dopaminergic neuronal activity and contribute to the control of prolactin (PRL) release. This study examined tyrosine hydroxylase mRNA signal levels in the arcuate nucleus of the hypothalamus and tyrosine hydroxylase activity in the stalk-median eminence after 1 week of steroid treatment and related these to circulating PRL levels. Ovariectomized rats were untreated (control) or were implanted with E<sub>2</sub>, P<sub>4</sub> or both E<sub>2</sub> and P<sub>4</sub> pellets and were sacrificed after 7 days at either 10:00 or 18:00 h. Some E<sub>2</sub>+P<sub>4</sub>-treated rats were injected with either RU 486 or its vehicle at 12-hour intervals for the last 3 of the 7 days of steroid treatment. Tyrosine hydroxylase mRNA signal levels in the arcuate nucleus were decreased by 70% at both 10:00 and 18:00 h in the E<sub>2</sub>-treated rats compared to control rats. P<sub>4</sub> alone had no effect on tyrosine hydroxylase mRNA levels, but reversed the E<sub>2</sub>-induced decrease so that mRNA levels in the E<sub>2</sub>+P<sub>4</sub>-treated rats were similar to control levels. The progesterone antagonist RU 486 blocked this effect of P<sub>4</sub>, supporting the observation of decreased mRNA levels in E<sub>2</sub>-treated rats. Steroid treatment had no effect on tyrosine hydroxylase mRNA levels in the medial zona incerta. Tyrosine hydroxylase activity in the stalk-median eminence was similar at 10:00 and 18:00 h in control rats, and was decreased by 25 and 36% at 10:00 and 18:00 h, respectively, in E<sub>2</sub>-treated rats. P<sub>4</sub> alone had no effect on tyrosine hydroxylase activity, but reversed the E<sub>2</sub>-induced decrease in enzyme activity to control levels at both 10:00 and 18:00 h. In contrast to the effect of RU 486 on tyrosine hydroxylase mRNA, tyrosine hydroxylase activity in E<sub>2</sub>+P4-treated rats was not significantly altered by RU 486 at either 10:00 or 18:00 h. Circulating PRL levels were elevated in the E<sub>2</sub>-treated and E<sub>2</sub>+P<sub>4</sub>-treated rats. A diurnal PRL rise was evident at 18:00 h in E<sub>2</sub>-treated rats, but was abolished by concomitant treatment with P<sub>4</sub>. The diurnal PRL surge was re-established in E<sub>2</sub>+P4-treated rats after administration of RU 486, whereas basal circulating PRL levels were not altered by RU 486. These data indicate that P4 antagonizes the profound inhibitory effect or E<sub>2</sub> on tyrosine hydroxylase mRNA content in the tuberoinfundibular dopaminergic neurons. However, since tyrosine hydroxylase activity is only modestly reduced and exhibits a diurnal rhythm in E<sub>2</sub>-treated rats, the regulation of enzyme activity likely is dependent on additional inputs. Although a decrease in tuberoinfundibular dopaminergic neuronal activity may contribute to elevated PRL levels in E<sub>2</sub>-treated rats, it is likely not the primary drive for the diurnal E<sub>2</sub>-induced PRL surge.

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          Author and article information

          S. Karger AG
          08 April 2008
          : 58
          : 5
          : 501-510
          Department of Physiology, University of Kansas Medical Center, Kansas City, Kans., USA
          126583 Neuroendocrinology 1993;58:501–510
          © 1993 S. Karger AG, Basel

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          Page count
          Pages: 10
          Regulation of Hypothalamic Neurons


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