Control of the Ovarian Cycle of the Sheep

Goodman, Robert L.; Inskeep, E. K.

doi:10.1016/b978-0-12-397175-3.00027-2

Cited by 33 publications

(27 citation statements)

References 335 publications

(417 reference statements)

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“…These neurons could receive direct input from PR-OFQ/N neurons located in the AVPV (aka RP3V), MPN or even a population of ARH PR-PFQ/N neurons. Further, it is possible that ORL-1 activation is compartmentalized within the ARH for ovarian steroids to act through OFQ/N to regulate β-END release that modulates GnRH release [83]. Like the rodent, infusion of OFQ/N into the lateral ventricle of the ewe reduced LH secretion, and appear to regulate LH pulse frequency and amplitude [73].…”

Section: Discussionmentioning

confidence: 99%

“…Ovarian hormone modulation of pre- and postsynaptic ORL-1 signaling that regulates neuronal activity of POMC neurons indicates that the OFQ/N-ORL-1 system could play an important role in synchronizing multiple homeostatic, reproductive and behavioral systems in addition to sexual receptivity that is controlled by products of the POMC gene [1, 55, 83]. …”

Section: Discussionmentioning

confidence: 99%

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Estradiol Upregulates Progesterone Receptor and Orphanin FQ Colocalization in Arcuate Nucleus Neurons and Opioid Receptor-Like Receptor-1 Expression in Proopiomelanocortin Neurons That Project to the Medial Preoptic Nucleus in the Female Rat

Sanathara

Moreas²,

Mahavongtrakul³

et al. 2014

Neuroendocrinology

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Background: Ovarian steroids regulate sexual receptivity in the female rat by acting on neurons that converge on proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARH) that project to the medial preoptic nucleus (MPN). Estradiol rapidly activates these neurons to release β-endorphin that activates MPN μ-opioid receptors (MOP) to inhibit lordosis. Lordosis is facilitated by the subsequent action of progesterone that deactivates the estradiol-induced MPN MOP activation. Orphanin FQ (OFQ/N; also known as nociceptin) infusions into the ARH, like progesterone, deactivate MPN MOP and facilitate lordosis in estradiol-primed rats. OFQ/N reduces the activity of ARH β-endorphin neurons through post- and presynaptic mechanisms via its cognate receptor, ORL-1. Methods: We tested the hypotheses that progesterone receptors (PR) are expressed in ARH OFQ/N neurons by immunohistochemistry and ORL-1 is expressed in POMC neurons that project to the MPN by combining Fluoro-Gold injection into the MPN and double-label fluorescent in situ hybridization (FISH). We also hypothesized that estradiol increases coexpression of PR-OFQ/N and ORL-1-POMC in ARH neurons of ovariectomized rats. Results: The number of PR- and OFQ/N-immunopositive ARH neurons was increased as was their colocalization by estradiol treatment. FISH for ORL-1 and POMC mRNA revealed a subpopulation of ARH neurons that was triple labeled, indicating these neurons project to the MPN and coexpress ORL-1 and POMC mRNA. Estradiol was shown to upregulate ORL-1 and POMC expression in MPN-projecting ARH neurons. Conclusion: Estradiol upregulates the ARH OFQ/N-ORL-1 system projecting to the MPN that regulates lordosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Estradiol Upregulates Progesterone Receptor and Orphanin FQ Colocalization in Arcuate Nucleus Neurons and Opioid Receptor-Like Receptor-1 Expression in Proopiomelanocortin Neurons That Project to the Medial Preoptic Nucleus in the Female Rat

Sanathara

Moreas²,

Mahavongtrakul³

et al. 2014

Neuroendocrinology

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“…The output of the pulse generator, on the other hand, is relayed from the midline arcuate nucleus to the more lateral and basal network of GnRH neurons by release of kisspeptin from axonal terminals originating from KNDy neurons. It should be noted that the model does not exclude the possibility that other neurons in the arcuate nucleus, such as glutamate inter neurons are an important component of pulse generation ([45], [46]). Moreover, for the model to be comprehensive it will also need to incorporate earlier findings indicating the importance of noreadrenergic and neuropeptide Y signaling to GnRH pulse generation ([47] [48] [49]).…”

Section: The Hypothalamic Gnrh Pulse Generatormentioning

confidence: 99%

Neuroendocrine control of the onset of puberty

Plant

2015

Frontiers in Neuroendocrinology

170

144

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This chapter is based on the Geoffrey Harris Memorial Lecture presented at the 8th International Congress of Neuroendocrinology, which was held in Sydney, August 2014. It provides the development of our understanding of the neuroendocrine control of puberty since Harris proposed in his 1955 monograph [2] that “a major factor responsible for puberty is an increased rate of release of pituitary gonadotrophin” and posited “that a neural (hypothalamic) stimulus, via the hypophysial portal vessels, may be involved.” Emphasis is placed on the neurobiological mechanisms governing puberty in highly evolved primates, although an attempt is made to reverse translate a model for the timing of puberty in man and monkey to non-primate species.

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“…In contrast to dynorphin, neurokinin B is generally stimulatory to GnRH release. Additional information obtained over the last decade has permitted the formulation of a model for GnRH pulse generation (Figure 5) that posits this hypothalamic timing mechanism is initiated in the KNDy neuronal network of the arcuate nucleus by a reciprocating interplay of stimulatory neurokinin B signals and inhibitory dynorphin inputs (Rance, et al 2010) (Wakabayashi, et al 2010) (Goodman 2015). As mentioned above, the output of the pulse generator is posited to be relayed from the arcuate nucleus to the GnRH neuronal network by release of kisspeptin from axonal terminals originating from KNDy neurons.…”

Section: Neurobiology Of the Hypothalamic Gnrh Pulse Generatormentioning

confidence: 99%

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

Plant

2015

Journal of Endocrinology

208

125

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This review provides an outline of how our understanding of the neuroendocrine control of the hypothalamo-pituitary–gonadal axis has evolved since the publication of Geoffrey Harris' renowned monograph in 1955. Particular attention is directed to the neurobiology underlying pulsatile GnRH release from the hypothalamus, the neuroendocrine control of ovarian cycles, puberty and seasonality of gonadal function, and to ideas that have emerged as a result of examining the relationship between growth and the reproductive axis. The review closes with i) a brief discussion of how knowledge gained as a result of pursing the early hypotheses of Harris has led to major clinical and therapeutic applications, and ii) a personal glimpse into the future of research in this fascinating area of biology.

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Control of the Ovarian Cycle of the Sheep

Cited by 33 publications

References 335 publications

Estradiol Upregulates Progesterone Receptor and Orphanin FQ Colocalization in Arcuate Nucleus Neurons and Opioid Receptor-Like Receptor-1 Expression in Proopiomelanocortin Neurons That Project to the Medial Preoptic Nucleus in the Female Rat

Estradiol Upregulates Progesterone Receptor and Orphanin FQ Colocalization in Arcuate Nucleus Neurons and Opioid Receptor-Like Receptor-1 Expression in Proopiomelanocortin Neurons That Project to the Medial Preoptic Nucleus in the Female Rat

Neuroendocrine control of the onset of puberty

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

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