Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques

Melanie Pecins-Thompson, Nancy A. Brown, Steven Kohama, Cynthia Bethea

    Research output: Contribution to journalArticle

    141 Citations (Scopus)

    Abstract

    Progesterone (P) stimulates prolactin secretion through an unknown neural mechanism in estrogen (E)-primed female monkeys. Serotonin is a stimulatory neurotransmitter in prolactin regulation, and this laboratory has shown previously that E induces progestin receptors (PR) in serotonin neurons. Therefore, we questioned whether E and/or E + P increased serotonin neural function. The expression of mRNA for tryptophan hydroxylase (TPH) was examined in ovariectomized (spayed) control, E-treated (28 d), and E+P- treated monkeys (14 d E and 14 d E+P) using in situ hybridization and a 249 bp TPH cRNA probe generated with RT-PCR (n = 5 animals/group). Densitometric analysis of film autoradiographs revealed a ninefold increase in TPH mRNA in E-treated macaques compared to spayed animals (p <0.05). With supplemental P treatment, TPH mRNA signal was increased fivefold over spayed animals (p <0.05), but was not significantly different compared to E-treated animals. These results were verified by grain counts from photographic emulsion- coated slides. There were significantly higher single-cell levels of TPH mRNA in serotonergic neurons of the dorsal raphe in E- and E+P-treated groups (p <0.05). These data indicate that E induces TPH gene expression in nonhuman primates and that the addition of P has little additive effect on TPH gene expression. Thus, the action of P on prolactin secretion is probably not mediated at the level of TPH gene transcription. However, because P increases raphe serotonin content in E-primed rodents, the possibility remains that P may have other actions on post-translational processing or enzyme activity.

    Original languageEnglish (US)
    Pages (from-to)7021-7029
    Number of pages9
    JournalJournal of Neuroscience
    Volume16
    Issue number21
    StatePublished - Nov 1 1996

    Fingerprint

    Tryptophan Hydroxylase
    Macaca mulatta
    Steroids
    Messenger RNA
    Serotonin
    Prolactin
    Haplorhini
    Serotonergic Neurons
    Gene Expression
    Complementary RNA
    Macaca
    Progesterone Receptors
    Emulsions
    Primates
    In Situ Hybridization
    Progesterone
    Neurotransmitter Agents
    Rodentia
    Estrogens
    Neurons

    Keywords

    • dorsal raphe
    • estrogen
    • monkey
    • progesterone
    • serotonin
    • tryptophan hydroxylase mRNA

    ASJC Scopus subject areas

    • Neuroscience(all)

    Cite this

    Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques. / Pecins-Thompson, Melanie; Brown, Nancy A.; Kohama, Steven; Bethea, Cynthia.

    In: Journal of Neuroscience, Vol. 16, No. 21, 01.11.1996, p. 7021-7029.

    Research output: Contribution to journalArticle

    Pecins-Thompson, M, Brown, NA, Kohama, S & Bethea, C 1996, 'Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques', Journal of Neuroscience, vol. 16, no. 21, pp. 7021-7029.
    Pecins-Thompson, Melanie ; Brown, Nancy A. ; Kohama, Steven ; Bethea, Cynthia. / Ovarian steroid regulation of tryptophan hydroxylase mRNA expression in rhesus macaques. In: Journal of Neuroscience. 1996 ; Vol. 16, No. 21. pp. 7021-7029.
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    abstract = "Progesterone (P) stimulates prolactin secretion through an unknown neural mechanism in estrogen (E)-primed female monkeys. Serotonin is a stimulatory neurotransmitter in prolactin regulation, and this laboratory has shown previously that E induces progestin receptors (PR) in serotonin neurons. Therefore, we questioned whether E and/or E + P increased serotonin neural function. The expression of mRNA for tryptophan hydroxylase (TPH) was examined in ovariectomized (spayed) control, E-treated (28 d), and E+P- treated monkeys (14 d E and 14 d E+P) using in situ hybridization and a 249 bp TPH cRNA probe generated with RT-PCR (n = 5 animals/group). Densitometric analysis of film autoradiographs revealed a ninefold increase in TPH mRNA in E-treated macaques compared to spayed animals (p <0.05). With supplemental P treatment, TPH mRNA signal was increased fivefold over spayed animals (p <0.05), but was not significantly different compared to E-treated animals. These results were verified by grain counts from photographic emulsion- coated slides. There were significantly higher single-cell levels of TPH mRNA in serotonergic neurons of the dorsal raphe in E- and E+P-treated groups (p <0.05). These data indicate that E induces TPH gene expression in nonhuman primates and that the addition of P has little additive effect on TPH gene expression. Thus, the action of P on prolactin secretion is probably not mediated at the level of TPH gene transcription. However, because P increases raphe serotonin content in E-primed rodents, the possibility remains that P may have other actions on post-translational processing or enzyme activity.",
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