Further evidence that luteinizing hormone-releasing hormone also is follicle-stimulating hormone-releasing hormone

P. M. Wise, Naomi E Rance, G. D. Barr, C. A. Barraclough

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

While LHRH evokes the release of both LH and FSH under a wide spectrum of experimental conditions, this hormone has not been shown to induce the discharge of FSH unaccompanied by LH release. As a consequence, the possibility that a separate FSHRH exists has not been discounted. These experiments were designed to demonstrate that LHRH is capable of promoting marked increase in plasma FSH concomitant with physiologically insignificant changes in plasma LH and, thus, that LHRH is also FSHRH. Seven groups of cyclic female rats received phenobarbital at 1200 h proestrus to block spontaneous preovulatory LH and FSH surges. These various groups then were subdivided according to whether phosphate-buffered saline (PBS), LHRH, or both was infused (iv). The experimental protocol consisted of infusing material for an initial 30 min (priming period), stopping the infusion for 30 min (rest interval), and again infusing for an additional 210 min (maintenance period). When PBS were infused during the priming and maintenance periods, plasma LH and FSH remained basal. In contrast, when a total of 25 ng LHRH was infused during the first 30 min, followed by the infusion of a total of 17.5 ng LHRH during the 210-min maintenance period, plasma FSH concentrations increased to levels comparable to those observed during the proestrous preovulatory FSH surge. In these animals, plasma LH increased to only 8% of proestrous values, which was insufficient to alter plasma estradiol and progesterone concentrations 60 min after the beginning of the initial LHRH infusion period. When the priming dose of LHRH was decreased by 50% (12.5 ng), the peak plasma FSH concentrations, which were induced by infusing 17.5 ng LHRH during the maintenance period, also were halved. Infusion of LHRH only during the priming or maintenance period did not appreciably affect basal plasma FSH concentrations. In Nembutal-blocked proestrous rats, low intensity electrical stimulation of the preoptic area was performed in an attempt to induce the endogenous release of LHRH in patterns and concentrations similar to those produced by the infusion protocol. Such stimuli induced the selective increase in plasma FSH. To the authors' knowledge, these studies are the first to demonstrate that synthetic LHRH or medial preoptic area electrical stimulation can induce marked increase in plasma FSH without prior or simultaneous large increments in plasma LH; thus, they provide additional evidence that LHRH also is FSHRH.

Original languageEnglish (US)
Pages (from-to)940-947
Number of pages8
JournalEndocrinology
Volume104
Issue number4
StatePublished - 1979
Externally publishedYes

Fingerprint

Follicle Stimulating Hormone
Gonadotropin-Releasing Hormone
Hormones
Maintenance
Preoptic Area
Electric Stimulation
Phosphates
Proestrus
Pentobarbital
Phenobarbital
Progesterone
Estradiol

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Further evidence that luteinizing hormone-releasing hormone also is follicle-stimulating hormone-releasing hormone. / Wise, P. M.; Rance, Naomi E; Barr, G. D.; Barraclough, C. A.

In: Endocrinology, Vol. 104, No. 4, 1979, p. 940-947.

Research output: Contribution to journalArticle

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abstract = "While LHRH evokes the release of both LH and FSH under a wide spectrum of experimental conditions, this hormone has not been shown to induce the discharge of FSH unaccompanied by LH release. As a consequence, the possibility that a separate FSHRH exists has not been discounted. These experiments were designed to demonstrate that LHRH is capable of promoting marked increase in plasma FSH concomitant with physiologically insignificant changes in plasma LH and, thus, that LHRH is also FSHRH. Seven groups of cyclic female rats received phenobarbital at 1200 h proestrus to block spontaneous preovulatory LH and FSH surges. These various groups then were subdivided according to whether phosphate-buffered saline (PBS), LHRH, or both was infused (iv). The experimental protocol consisted of infusing material for an initial 30 min (priming period), stopping the infusion for 30 min (rest interval), and again infusing for an additional 210 min (maintenance period). When PBS were infused during the priming and maintenance periods, plasma LH and FSH remained basal. In contrast, when a total of 25 ng LHRH was infused during the first 30 min, followed by the infusion of a total of 17.5 ng LHRH during the 210-min maintenance period, plasma FSH concentrations increased to levels comparable to those observed during the proestrous preovulatory FSH surge. In these animals, plasma LH increased to only 8{\%} of proestrous values, which was insufficient to alter plasma estradiol and progesterone concentrations 60 min after the beginning of the initial LHRH infusion period. When the priming dose of LHRH was decreased by 50{\%} (12.5 ng), the peak plasma FSH concentrations, which were induced by infusing 17.5 ng LHRH during the maintenance period, also were halved. Infusion of LHRH only during the priming or maintenance period did not appreciably affect basal plasma FSH concentrations. In Nembutal-blocked proestrous rats, low intensity electrical stimulation of the preoptic area was performed in an attempt to induce the endogenous release of LHRH in patterns and concentrations similar to those produced by the infusion protocol. Such stimuli induced the selective increase in plasma FSH. To the authors' knowledge, these studies are the first to demonstrate that synthetic LHRH or medial preoptic area electrical stimulation can induce marked increase in plasma FSH without prior or simultaneous large increments in plasma LH; thus, they provide additional evidence that LHRH also is FSHRH.",
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T1 - Further evidence that luteinizing hormone-releasing hormone also is follicle-stimulating hormone-releasing hormone

AU - Wise, P. M.

AU - Rance, Naomi E

AU - Barr, G. D.

AU - Barraclough, C. A.

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N2 - While LHRH evokes the release of both LH and FSH under a wide spectrum of experimental conditions, this hormone has not been shown to induce the discharge of FSH unaccompanied by LH release. As a consequence, the possibility that a separate FSHRH exists has not been discounted. These experiments were designed to demonstrate that LHRH is capable of promoting marked increase in plasma FSH concomitant with physiologically insignificant changes in plasma LH and, thus, that LHRH is also FSHRH. Seven groups of cyclic female rats received phenobarbital at 1200 h proestrus to block spontaneous preovulatory LH and FSH surges. These various groups then were subdivided according to whether phosphate-buffered saline (PBS), LHRH, or both was infused (iv). The experimental protocol consisted of infusing material for an initial 30 min (priming period), stopping the infusion for 30 min (rest interval), and again infusing for an additional 210 min (maintenance period). When PBS were infused during the priming and maintenance periods, plasma LH and FSH remained basal. In contrast, when a total of 25 ng LHRH was infused during the first 30 min, followed by the infusion of a total of 17.5 ng LHRH during the 210-min maintenance period, plasma FSH concentrations increased to levels comparable to those observed during the proestrous preovulatory FSH surge. In these animals, plasma LH increased to only 8% of proestrous values, which was insufficient to alter plasma estradiol and progesterone concentrations 60 min after the beginning of the initial LHRH infusion period. When the priming dose of LHRH was decreased by 50% (12.5 ng), the peak plasma FSH concentrations, which were induced by infusing 17.5 ng LHRH during the maintenance period, also were halved. Infusion of LHRH only during the priming or maintenance period did not appreciably affect basal plasma FSH concentrations. In Nembutal-blocked proestrous rats, low intensity electrical stimulation of the preoptic area was performed in an attempt to induce the endogenous release of LHRH in patterns and concentrations similar to those produced by the infusion protocol. Such stimuli induced the selective increase in plasma FSH. To the authors' knowledge, these studies are the first to demonstrate that synthetic LHRH or medial preoptic area electrical stimulation can induce marked increase in plasma FSH without prior or simultaneous large increments in plasma LH; thus, they provide additional evidence that LHRH also is FSHRH.

AB - While LHRH evokes the release of both LH and FSH under a wide spectrum of experimental conditions, this hormone has not been shown to induce the discharge of FSH unaccompanied by LH release. As a consequence, the possibility that a separate FSHRH exists has not been discounted. These experiments were designed to demonstrate that LHRH is capable of promoting marked increase in plasma FSH concomitant with physiologically insignificant changes in plasma LH and, thus, that LHRH is also FSHRH. Seven groups of cyclic female rats received phenobarbital at 1200 h proestrus to block spontaneous preovulatory LH and FSH surges. These various groups then were subdivided according to whether phosphate-buffered saline (PBS), LHRH, or both was infused (iv). The experimental protocol consisted of infusing material for an initial 30 min (priming period), stopping the infusion for 30 min (rest interval), and again infusing for an additional 210 min (maintenance period). When PBS were infused during the priming and maintenance periods, plasma LH and FSH remained basal. In contrast, when a total of 25 ng LHRH was infused during the first 30 min, followed by the infusion of a total of 17.5 ng LHRH during the 210-min maintenance period, plasma FSH concentrations increased to levels comparable to those observed during the proestrous preovulatory FSH surge. In these animals, plasma LH increased to only 8% of proestrous values, which was insufficient to alter plasma estradiol and progesterone concentrations 60 min after the beginning of the initial LHRH infusion period. When the priming dose of LHRH was decreased by 50% (12.5 ng), the peak plasma FSH concentrations, which were induced by infusing 17.5 ng LHRH during the maintenance period, also were halved. Infusion of LHRH only during the priming or maintenance period did not appreciably affect basal plasma FSH concentrations. In Nembutal-blocked proestrous rats, low intensity electrical stimulation of the preoptic area was performed in an attempt to induce the endogenous release of LHRH in patterns and concentrations similar to those produced by the infusion protocol. Such stimuli induced the selective increase in plasma FSH. To the authors' knowledge, these studies are the first to demonstrate that synthetic LHRH or medial preoptic area electrical stimulation can induce marked increase in plasma FSH without prior or simultaneous large increments in plasma LH; thus, they provide additional evidence that LHRH also is FSHRH.

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