The Role of Catecholamines in the Regulation of Pituitary Luteinizing Hormone and Follicle-Stimulating Hormone Secretion

Barraclough, Charles A.; Wise, Phyllis M.

doi:10.1210/edrv-3-1-91

Cited by 402 publications

(153 citation statements)

References 138 publications

(218 reference statements)

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“…Pharmacological manipulation of various neurotransmitter and peptidergic systems has been shown to affect GnRH and subsequent LH release in female mammals. Most of this work has been done in spontaneous ovulators, including rats (9,25,93,133,153) and monkeys (reviewed in 208). To date, the rabbit (reviewed in 179,208) and ferret (120,229) are the only induced ovulating species in which pharmacological studies have been conducted to analyze the neuroendocrine signals which control the postcoital release of GnRH from the MBH.…”

Section: Neurotransmitters and Neuropeptides Involved In The Preovulamentioning

confidence: 99%

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Bakker

Baum

2000

Frontiers in Neuroendocrinology

180

135

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GnRH is the key neuropeptide controlling reproductive function in all vertebrate species. Two different neuroendocrine mechanisms have evolved among female mammals to regulate the mediobasal hypothalamic (MBH) release of GnRH leading to the preovulatory secretion of LH by the anterior pituitary gland. In females of spontaneously ovulating species, including rats, mice, guinea pigs, sheep, monkeys, and women, ovarian steroids secreted by maturing ovarian follicles induce a pulsatile pattern of GnRH release in the median eminence that, in turn, stimulates a preovulatory LH surge. In females of induced ovulating species, including rabbits, ferrets, cats, and camels, the preovulatory release of GnRH, and the resultant preovulatory LH surge, is induced by the receipt of genital somatosensory stimuli during mating. Induced ovulators generally do not show "spontaneous" steroid-induced LH surges during their reproductive cycles, suggesting that the positive feedback actions of steroid hormones on GnRH release are reduced or absent in these species. By contrast, mating-induced preovulatory surges occasionally occur in some spontaneously ovulating species. Most research in the field of GnRH neurobiology has been performed using spontaneous ovulators including rat, guinea pig, sheep, and rhesus monkey. This review summarizes the literature concerning the neuroendocrine mechanisms controlling GnRH biosynthesis and release in females of several induced ovulating species, and whenever possible it contrasts the results with those obtained for spontaneously ovulating species. It also considers the adaptive, evolutionary benefits and disadvantages of each type of ovulatory control mechanism. In females of induced ovulating species estradiol acts in the brain to induce aspects of proceptive and receptive sexual behavior. The primary mechanism involved in the preovulatory release of GnRH among induced ovulators involves the activation of midbrain and brainstem noradrenergic neurons in response to genital-somatosensory signals generated by receipt of an intromission from a male during mating. These noradrenergic neurons project to the MBH and, when activated, promote the release of GnRH from nerve terminals in the median eminence. In contrast to spontaneous ovulators, there is little evidence that endogenous opioid peptides normally inhibit MBH GnRH release among induced ovulators. Instead, the neural signals that induce a preovulatory LH surge in these species seem to be primarily excitatory. A complete understanding of the neuroendocrine control of ovulation will only be achieved in the future by comparative studies of several animal model systems in which mating-induced as well as spontaneous, hormonally stimulated activation of GnRH neurons drives the preovulatory LH surge. KEY WORDS: GnRH; MBH; induced ovulators; neuroendocrine regulation; preovulatory LH surge; spontaneous ovulators. © 2000 Academic Press Address correspondence and reprint requests to M. J. Baum at Dept. Biology, Boston University, 5 Cummington Street, Boston...

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Section: Neurotransmitters and Neuropeptides Involved In The Preovulamentioning

confidence: 99%

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Bakker

Baum

2000

Frontiers in Neuroendocrinology

180

135

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“…In relation to this, the POA is innervated by neurons containing the catecholamine neurotransmitters noradrenaline (NA; 7, 8) adrenaline (A; 9) and dopamine (DA; 10) and the inhibitory amino-acid y-aminobutyric acid (GABA; 1 I , 12). NA and GABA neurons have been shown to concentrate oestrogen (1 3-1 5 ) and all four neuroactive substances have been implicated in mediating the actions of gonadal steroids on LH secretion (16,17). This study sought to determine whether POA catecholamines and GABA play a role in mediating the actions of oestrogen on LH secretion during the preovulatory LH surge.…”

Section: Introductionmentioning

confidence: 99%

Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Robinson

Kendrick

Lambart

1991

J Neuroendocrinology

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The technique of intracranial microdialysis was used to monitor changes in the outflow of the catecholamines, noradrenaline, adrenaline and dopamine and the inhibitory amino-acid y-arninobutyric acid (GABA) in the preopticlseptal area of the conscious ewe during an oestradiol-induced surge of luteinizing hormone (LH). The s a m e animals were sampled twice from an identical brain site, once in the presence of oestradiol and once in its absence, when no surge occurred and LH levels remained low. Changes in the outflow of GABA, noradrenaline and adrenaline (but not dopamine) were related to changes in LH secretion. Specifically, GABA outflow was maximal in the h o u r s following oestradiol administration but began a sustained fall some 10 h before the surge began, to level off just before the first increment in LH secretion. Low GABA concentrations were maintained until after gonadotrophin levels had once more returned to baseline. The release of all three catecholamines was pulsatile. Noradrenergic activity was greater in the presence of oestradiol although activity did not alter over t h e 20 h of sampling. The pulse frequency of adrenaline was maximal in the h o u r s immediately prior to the LH surge and minimal in the hours following its initiation. These data suggest that a decrease in GABAergic transmission in t h e vicinity of t h e LH-releasing hormone cell bodies is a necessary component of the neural mechanism by which the oestradiol-induced surge of LH is generated. A general increase in noradrenergic activity coupled with changes in the release of adrenaline at t h e time of the surge may be additional prerequisites for successful ovulation.The hormonal events which are required to elicit the massive increment in luteinizing hormone (LH) secretion necessary to cause ovulation are relatively well understood and allow us, to some degree, to manipulate both our own fertility and that of other species ( I , 2). In contrast, the neural events which are a prerequisite for the LH surge remain largely enigmatic.Our knowledge has recently been extended by data demonstrating conclusively that the oestradiol-induced LH surge in the ewe results from a massive increase in the secretion of LH-releasing hormone (LHRH) into the portal vessels from nerve terminals located in the median eminence (3, 4). The cell bodies of these LHRH neurons are located in the preoptic and septa1 areas (POA/S) of the ovine brain ( 5 ) but as these cells d o not themselves possess oestrogen receptors (6), other steroid-sensitive neural elements must mediate oestrogen effects on LH. In relation to this, the POA is innervated by neurons containing the catecholamine neurotransmitters noradrenaline (NA; 7, 8) adrenaline (A; 9) and dopamine (DA; 10) and the inhibitory amino-acid y-aminobutyric acid (GABA; 1 I , 12). NA and GABA neurons have been shown to concentrate oestrogen (1 3-1 5 ) and all four neuroactive substances have been implicated in mediating the actions of gonadal steroids on LH secretion (16,17). This study sought to d...

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“…A II excites a large proportion of neurons in this region, increasing the neuronal discharge frequency (13) and facilitating the release of norepinephrine and dopamine (12) in the MPOA. Norepinephrine is released in a pulsatile pattern and stimulates LHRH secretion (11).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, norepinephrine has a stimulatory action on LH secretion (11). Furthermore, there is an interaction between A II and catecholamines in certain brain structures (3), among them the MPOA, where A II facilitates the release of norepinephrine and dopamine (12).…”

Section: Introductionmentioning

confidence: 99%

Alpha- but not beta-adrenergic receptors mediate the effect of angiotensin II in the medial preoptic area on gonadotropin and prolactin secretion

Dornelles

Franci

1998

European Journal of Endocrinology

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The aim of this work was to study the participation of a-and b-adrenergic receptors on the effect of microinjection of angiotensin II (A II) into the medial preoptic area (MPOA) on the secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) in estrogen-primed ovariectomized (OVX) rats. Microinjection of A II into the MPOA increased plasma LH. This effect was reduced by previous microinjection of an a-(phentolamine), but not a b-(propranolol) adrenergic blocker into the MPOA. Plasma PRL decreased after microinjection of A II into the MPOA, but this effect was unchanged by phentolamine or propranolol. There was no change in plasma FSH in any condition. These results indicate that A II in the MPOA stimulates LH secretion and inhibits PRL secretion in estrogen-primed OVX rats. The effect on secretion of LH, but not of PRL, is mediated by aadrenergic receptors in the MPOA.

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The Role of Catecholamines in the Regulation of Pituitary Luteinizing Hormone and Follicle-Stimulating Hormone Secretion

Cited by 402 publications

References 138 publications

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Alpha- but not beta-adrenergic receptors mediate the effect of angiotensin II in the medial preoptic area on gonadotropin and prolactin secretion

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