Gonad hormone functions, and the reciprocal influence between gonads and hypophysis with its bearing on the problem of sex hormone antagonism

Moore, Carl R.; Price, Dorothy

doi:10.1002/aja.1000500103

Cited by 285 publications

(41 citation statements)

References 69 publications

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“…17␤-Estradiol (E2) regulates multiple neuronal functions, including neurogenesis (McEwen et al, 2001), reproductive behavior (Meisel and Sachs, 1994), and neuroendocrine output (Moore and Price, 1932;Levine et al, 1985). The classical mechanism of E2 action is through intracellular estrogen receptors (ERs), ER␣ and ER␤, acting as transcription factors (Kuiper et al, 1996).…”

Section: Introductionsupporting

confidence: 47%

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Temple¹,

Laing²,

Sunder³

et al. 2004

J. Neurosci.

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Pulsatile secretion of gonadotropin-releasing hormone-1 (GnRH-1) is essential for reproduction. GnRH-1 induces gonadotropin release and is regulated by 17␤-estradiol (E2). Although a subpopulation of GnRH-1 neurons expresses estrogen receptor (ER) ␤, it is unclear whether E2 acts directly on GnRH-1 neurons or indirectly through interneuronal connections. To test the hypothesis that E2 acts directly on GnRH-1 neurons to regulate neuronal activity, we used calcium imaging to monitor intracellular calcium oscillations in GnRH-1 neurons maintained in nasal explants. TTX was used to minimize synaptic input from other cells. Consistent with previous studies, TTX reduced the activity of individual GnRH-1 neurons to a basal level, while the population of cells maintained synchronized calcium oscillations. Exposure of GnRH-1 cells to TTX plus E2 increased the number of calcium peaks/cell, percentage of cells with Ն10 peaks, mean peak amplitude, and percentage of cells that contributed to each calcium pulse in explants maintained in vitro for 7 d (7 div) compared with TTX alone. These effects were induced within 30 min and were not mimicked by 17␣-estradiol, E2 conjugated to BSA (which does not cross the plasma membrane), or seen at 21 div, when the percentage of GnRH-1 cells expressing ER␤ transcripts declines. In addition, these effects were inhibited by the ER antagonist ICI 182,780 and prevented by inhibition of gene transcription. These data suggest that, via ER␤, E2 can rapidly act as a hormone-activated transcription complex and are the first to show that E2 directly increases GnRH-1 neuronal activity and synchronization.

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Section: Introductionsupporting

confidence: 47%

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Temple¹,

Laing²,

Sunder³

et al. 2004

J. Neurosci.

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“…HPA activity is tightly controlled via complex regulatory mechanisms of glucocorticoid negative feedback involving signaling networks at the pituitary, hypothalamus, and hippocampus (Watts, 2005). The underlying HPA control mechanism of endogenous cortisol feedback inhibition was first discovered by Moore and Price (1932). Although the basic tenet remains, there is new evidence that ultradian rhythmicity itself is attributable to an oscillatory feedforward-feedback relationship between the pituitary and adrenal gland (Walker et al, 2010).…”

Section: Introductionsupporting

confidence: 42%

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

Russell¹,

Henley²,

Leendertz³

et al. 2010

J. Neurosci.

106

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A complex dynamic ultradian rhythm underlies the hypothalamic-pituitary-adrenal (HPA) circadian rhythm. We have investigated in normal human male subjects the importance, site of action, and receptor-mediated processes involved in rapid basal corticosteroid feedback and its interaction with corticotrophin releasing hormone (CRH) drive. Pro-opiomelanocortin (POMC), ACTH, and cortisol were measured every 10 min from healthy males during the awakening period or late afternoon using an automated blood sampling system. Mathematical modeling into discrete pulses of activity revealed that intravenous infusion of the synthetic mixed glucocorticoid/ mineralocorticoid agonist prednisolone produced rapid inhibition of ACTH and cortisol pulsatility within 30 min in the morning and afternoon. Any pulse that had commenced at the time of injection was unaffected, and subsequent pulsatility was inhibited. Prednisolone also inhibited ACTH and cortisol secretion in response to exogenous CRH stimulation, inferring rapid feedback inhibition at the anterior pituitary. Circulating POMC peptide concentrations were unaffected, suggesting that the rapid corticosteroid inhibitory effect specifically targeted ACTH secretion from pituitary corticotrophs. Prednisolone fast feedback was only reduced by glucocorticoid receptor antagonist pretreatment and not by mineralocorticoid receptor antagonism, suggesting a glucocorticoid receptor-mediated pathway. The intravenous prednisolone suppression test provides a powerful new tool to investigate HPA abnormalities underlying metabolic and psychiatric disease states.

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“…Ovulation in many mammals is spontaneous and apparently regular, while in others genital stimulation is necessary to initiate the events leading to ovulation. The regular and cyclic event of spontaneous ovulation in rodents stimulated the discovery of the reciprocal relationship between the ovary and the pituitary (Moore & Price, 1932) and the central nervous system (Hohlweg & Junkman, 1932; for review see Barraclough, 1973).…”

Section: Introductionmentioning

confidence: 45%

Follicular Growth: The Basic Event in the Mouse and Human Ovary

Peters¹,

Byskov²,

et al. 1975

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Gonad hormone functions, and the reciprocal influence between gonads and hypophysis with its bearing on the problem of sex hormone antagonism

Cited by 285 publications

References 69 publications

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

Follicular Growth: The Basic Event in the Mouse and Human Ovary

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