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Chad D. Foradori

Researcher at Auburn University

Publications -  40
Citations -  1932

Chad D. Foradori is an academic researcher from Auburn University. The author has contributed to research in topics: Gonadotropin-releasing hormone & Luteinizing hormone. The author has an hindex of 22, co-authored 39 publications receiving 1749 citations. Previous affiliations of Chad D. Foradori include Colorado State University & University of Cincinnati.

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Non-genomic Actions of Androgens

TL;DR: The non-genomic effects of androgens are reviewed, along with a discussion of the possible role non- genomic androgen actions have on animal physiology and behavior.
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Estrogen receptor beta in the brain: From form to function

TL;DR: The studies implicate ERbeta as an important modulator of some non-reproductive neurobiological systems as well as the molecular and neuroanatomical targets of estrogen that are mediated by ERbeta remain to be determined.
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Colocalization of progesterone receptors in parvicellular dynorphin neurons of the ovine preoptic area and hypothalamus.

TL;DR: A dual-label immunoperoxidase procedure was used to visualize PRs and DYN in the preoptic area and hypothalamus of ovary-intact ewes killed during the luteal phase of the estrous cycle to test the hypothesis that an ultrashort feedback loop controls the release of DYN from ARC neurons.
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Colocalisation of dynorphin a and neurokinin B immunoreactivity in the arcuate nucleus and median eminence of the sheep.

TL;DR: Data suggest that a subpopulation of arcuate nucleus neurones coexpressing DYN and NKB mediate the negative feedback influence of progesterone on pulsatile GnRH secretion in the ewe and may also be involved in other feedback actions of gonadal steroids.
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Progesterone Increases Dynorphin A Concentrations in Cerebrospinal Fluid and Preprodynorphin Messenger Ribonucleic Acid Levels in a Subset of Dynorphin Neurons in the Sheep

TL;DR: Results are consistent with the hypothesis that progesterone acts via dynorphin neurons to inhibit pulsatile GnRH secretion and point to dynorph in neurons in the POA, AHA, and ARC as potential mediators of this action during the luteal phase.