Re-Evaluation of the Role of Catecholamines in Control of Gonadotropin and Prolactin Release

Vijayan, E.; McCann, Samuel M.

doi:10.1159/000122737

Cited by 169 publications

(59 citation statements)

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“…The presence of alpha adrenergic receptors has also been reported in the hypothalamic paraventricular, supraoptic and arcuate nuclei (Pascual et al 1992, Rosin et al 1996. Furthermore, epinephrine injected i.c.v., travels from the cerebral spinal fluid (CSF) to the hypothalamus and produces an increase in circulating LH; it is more effective than norepinephrine during a period of 30 min (Krieg & Sawyer 1976, Vijayan & McCann 1978, Gallo & Drouva 1979, Leung et al 1982, which is why epinephrine was used in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Doses of 4 to 25 µg norepinephrine or epinephrine administered i.c.v. usually produce an LH surge in peripheral blood after 10 to 20 min (Vijayan & McCann 1978, Krieg & Sawyer 1976, Donoso 1988. In this study, the smaller dose (0·5 µg) of epinephrine did not modify LH levels, but a larger amount of epinephrine (5 µg) injected i.c.v., as by these authors, raised the gonadotrophin level from 3 to 25 min in the jugular vein blood.…”

Section: Discussionmentioning

confidence: 99%

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Adrenergic intracerebroventricular stimulation affects progesterone concentration in the ovarian vein of the rat: participation of the superior ovarian nerve

Bortoli

Mh²,

Aguado³

1998

Journal of Endocrinology

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The present study investigates the acute consequences of central adrenergic stimulation on the release of steroids from the ovary. The influence of the superior ovarian nerve (SON) and the relationship between the neural effect and peripheral LH levels were also examined.The intracerebroventricular (i.c.v.) injection of 5 µg epinephrine in SON-intact rats on day 1 of dioestrus (D1) increased progesterone levels in ovarian vein blood from 7 to 21 min after injection but the same injection in SON-intact rats on day 2 of dioestrus (D2) decreased progesterone levels in ovarian vein blood from 1 to 25 min. A smaller dose (0·5 µg) of epinephrine injected i.c.v. in SON-intact rats produced a decrease in progesterone levels in ovarian vein blood of shorter duration. In SON-transected (SONt) animals, 0·5 µg epinephrine i.c.v. caused a smaller decrease in progesterone levels compared with SON-intact rats (P<0·05). On the other hand, in SON-intact rats on D2, the i.c.v. injection of 0·5 µg epinephrine did not modify the peripheral LH levels during 25 min, but 5 µg epinephrine injected i.c.v. raised the peripheral LH level from the third minute after injection (P<0·05). Oestradiol levels in the ovarian vein blood did not change after epinephrine i.c.v. injection in rats on D2.To avoid any humoral influence, SONt and SONintact rats on D2 were injected i.c.v. with 5 µg epinephrine or with vehicle, and 5 min later the ovaries were incubated in vitro with or without LH. Under these conditions, it was demonstrated that the previous injection of epinephrine in SON-intact rats resulted in a diminished release of progesterone from ovaries incubated with or without LH.These results suggest that a central adrenergic stimulus increases progesterone release from the ovary on D1 and decreases it on D2. Also, this neural input would arrive at the ovary through the SON, and would condition the ovarian response to LH on D2. Ovarian progesterone changes could be attributed to signals coming from ganglionar neurons, which are affected by the central adrenergic stimulation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Adrenergic intracerebroventricular stimulation affects progesterone concentration in the ovarian vein of the rat: participation of the superior ovarian nerve

Bortoli

Mh²,

Aguado³

1998

Journal of Endocrinology

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“…The regulation of pulsatile secretion of LH is complex and involves a number of neurotransmitters. Dopamine is thought by some investigators (21) to stimulate the secretion of LH, whereas others have provided evidence supporting an inhibitory effect (22,23). Gallo (22) has provided evidence that dopamine decreases the frequency of LH pulses.…”

Section: Discussionmentioning

confidence: 99%

Physiological role of alpha-melanocyte-stimulating hormone in modulating the secretion of prolactin and luteinizing hormone in the female rat.

Khorram¹,

Castro²,

McCann³

1984

Proc. Natl. Acad. Sci. U.S.A.

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Long-term ovariectomized (OVX) rats were injected in the third cerebral ventricle with 5 ,l~of the globulin fraction of an antiserum raised against a-melanocyte-stimulating hormone (a-MSH) or an equal volume of the globulin fraction of normal rabbit serum (NRS). Immunoneutralization of brain a-MSH produced an increase in the area under the secretion curve of prolactin (Prl), the amplitude of Prl pulses, and mean plasma Prl (P < 0.01). Recently, a-MSH has been found extensively throughout the brain, with high concentrations detected in axons and terminals of the hypophysiotropic area of the hypothalamus (4, 5). The cell bodies containing this peptide have been localized in the arcuate nucleus (5) and more recently in the dorsolateral region of the hypothalamus (6). Based on the distribution of this peptide and its detection in the hypophysial portal blood by a specific radioimmunoassay (RIA) (7), we evaluated the effect of this peptide on the release of anterior pituitary hormones.In recent studies we found that injection of a-MSH into the third ventricle of the brain of ovariectomized (OVX), freely moving rats produced a dose-dependent inhibition of basal and stress-induced release of prolactin (Prl) (8) and inhibited pulsatile release of luteinizing hormone (LH) (9). These effects could be blocked by prior administration of the inhibitor of catecholamine synthesis a-methyl-p-tyrosine or the dopamine receptor blocker spiroperidol (8, 9). a-MSH did not alter Prl and LH release from hemipituitaries and dispersed anterior pituitary cells incubated in vitro, which indicates that this peptide exerts its effect on Prl and LH release via an action in the hypothalamus to stimulate dopamine release, which, in turn, inhibits Prl and LH release (8,9). To determine whether the inhibitory effect of a-MSH may be physiologically relevant in the regulation of these hormones, we passively immunized rats with antisera to a-MSH. MATERIALS AND METHODSAdult female Sprague-Dawley rats of the Holtzman strain were employed. Females were OVX to eliminate the influence of ovarian steroids and elevate gonadotropin levels. The animals were used 3-6 weeks after ovariectomy. Antiserum was delivered to the brain via a cannula implanted in the third brain ventricle (10). A Silastic cannula implanted 24 hr before the experiment in the right external jugular vein (11) was used for withdrawal of blood samples (0.25 ml). After withdrawal of every sample, the blood volume was restored by an injection of an equal volume of heparinized (20 units/ ml), physiological saline. After every four samples, erythrocytes (0.5 ml) prepared previously were injected. The cells were obtained from OVX rats the day prior to the experiment and suspended in 0.9% saline to a hematocrit of 45%.The antiserum used (KDM-1) has been fully characterized (12). Briefly, this antiserum cross-reacts on a molar basis 0.029% with corticotropin (ACTH)-(1-24), 0.004% with ACTH-(1-39), 0.001% with ACTH-(1-10), and 36% with desacetyl-a-MSH and does not cross-react at a 100 mol...

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“…It is possible that this type of release is also partly under dopaminergic control because intraventricular injection of dopamine can increase LH release in the castrate (40). Furthermore, incubation of median eminence pieces from intact rats with dopamine can augment LHRH release and the response is blocked by pimozide, a dopamine receptor blocker (41).…”

Section: Putative Synaptic Transmitters Involved In Control Of Lhrh Rmentioning

confidence: 99%

Lh Releasing Hormone (Lhrh) -Past, Present and Future

McCann

1982

Folia Endocrinol

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It is a great honor to have the opportunity to address the Japanese Endocrine Society on the subject of a very important neuropeptide, LH-releasing hormone (LHRH). The following brief account will describe the development of our knowledge of LHRH from its discovery to the present time and suggest possible additional applications of the peptide in clinical medicine. LHRHLH-releasing activity was first found in hypothalamic extracts utilizing the ovarian ascorbic acid depletion assay of Parlow to measure LH released following injection of acid extracts of stalk-median eminence (1). At about the same time similarly prepared extracts were shown to evoke ovulation following intrapituitary injection (2). The activity was rapidly purified, shown to be a peptide on the basis of enzymatic degradation studies, and ultimately its structure was determined in Schally's laboratory by Matsuo and confirmed by synthesis (3). The elucidation of structure and synthesis of LHRH paved the way for its synthesis in large quantities which made possible clinical studies, many more physiological studies, the development of antisera which could be used to study the physiological significance of the peptide and the development of radioimmunoassay and immunocytochemical techniques to localize the peptide more precisely. Localization of LHRHIt is now clear on the basis of bioassay, radioimmunoassay and immunocytochemical localization that there are LHRH cell bodies in the septal-preoptic and anterior hypothalamic areas and that the axons of these neurons project particularly to the external layer of the anterior median eminence by passing caudally along a predominantly mediobasal course. The localization in the median eminence is presumably to permit release of LHRH into the hypophyseal portal capillaries. The axons also project to the organum vasculosum lamina terminalis (OVLT) and to more caudal structures (4). LHRH axons have been found even in brain stem regions thought to be involved in mating behavior (5). Recent evidence suggests that the distribution of LHRH and LHRH-like peptides is more widespread than originally thought and occurs throughout the reproductive system. LHRH has been found in the olfactory system by both immunoassay and immunocytochemistry (6). It has been found in testicular lymph by bioassay (7) and by immunocytochemistry in the interstitial cells of the testis (8). An LHRH-like peptide has been detected in ovarian extracts by bioassay and apparently is even produced by granulosa cells in culture (9). LHRH-like materials have

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Re-Evaluation of the Role of Catecholamines in Control of Gonadotropin and Prolactin Release

Cited by 169 publications

References 12 publications

Adrenergic intracerebroventricular stimulation affects progesterone concentration in the ovarian vein of the rat: participation of the superior ovarian nerve

Adrenergic intracerebroventricular stimulation affects progesterone concentration in the ovarian vein of the rat: participation of the superior ovarian nerve

Physiological role of alpha-melanocyte-stimulating hormone in modulating the secretion of prolactin and luteinizing hormone in the female rat.

Lh Releasing Hormone (Lhrh) -Past, Present and Future

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