Alpha Adrenergic Neurons Inhibit Luteinizing Hormone Pulse Amplitude in Breeding Season Ewes1

Goodman, Robert L.; Havern, R L; Whisnant, C.S.

doi:10.1095/biolreprod54.2.380

Cited by 16 publications

(12 citation statements)

References 42 publications

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“…Certainly, no substantial change in mean noradrenaline release was noted in the ovine preoptic area at the time of the GnRH surge, although the frequency of individual ‘episodes’ of noradrenaline release was observed to be greater just prior to the onset of the surge [12]. A case also exists for involvement of ovine noradrenergic cells in the negative-feedback action of estrogen within the GnRH network [7, 8, 9], although the precise pathways and mechanisms involved remain unknown and controversial. Scott et al [8] have suggested that the enhanced efficacy of estrogen to inhibit LH secretion in anestrus results, in part, from estrogen removing a stimulatory noradrenergic influence on GnRH neurons at this time.…”

Section: Discussionmentioning

confidence: 99%

“…Scott et al [8] have suggested that the enhanced efficacy of estrogen to inhibit LH secretion in anestrus results, in part, from estrogen removing a stimulatory noradrenergic influence on GnRH neurons at this time. In contrast, Havern et al [7] and Goodman et al [9] have suggested that estrogen may utilize noradrenergic neurons to inhibit, rather than stimulate, pulsatile LH secretion in both breeding-season and anestrous ewes. In future studies, it will be of interest to examine ER protein and mRNA expression in ovine noradrenergic neurons during the different seasons.…”

Section: Discussionmentioning

confidence: 99%

“…In the sheep, for example, noradrenergic fibers are found in close association with GnRH neurons [4, 5], and adrenergic antagonists block the occurrence of the luteinizing hormone (LH) surge [6]. Furthermore, direct infusion of noradrenaline into the preoptic area of the sheep, where most GnRH neurons are located, has been shown to modulate pulsatile LH secretion, depending on estrogen status and season [7, 8, 9]. However, in contrast to the rat [10, 11], the mean levels of noradrenaline release within the vicinity of the ovine GnRH cell bodies were not found to change during the estrogen-induced LH surge [12].…”

Section: Introductionmentioning

confidence: 99%

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Estrogen Receptor Expression in Brainstem Noradrenergic Neurons of the Sheep

et al. 1998

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Noradrenergic neurons are implicated in the estrogen-dependent neural regulation of luteinizing hormone secretion in a variety of mammalian species. The current study has used immunocytochemical methods to determine whether estrogen receptors (ER) are expressed within the brainstem of the ewe and to establish their relationship to noradrenergic neurons. Using a monoclonal mouse antiserum directed against the N-terminal of ERα, four distinct populations of ERα-immunoreactive cells were identified in ovine medulla and pons. The largest population was found in the superficial laminae of the spinal nucleus of the trigeminal nerve, followed by the nucleus tractus solitarius, lateral area postrema, and ventrolateral medulla. Double-labelling immunocytochemistry using antisera directed against the ERα and dopamine-β-hydroxylase revealed that noradrenergic neurons expressing ER immunoreactivity were only found in ventrolateral medulla (A1 cell group) and nucleus tractus solitarius (A2 cell group). No double-labelled cells were identified in the A5, A6, or A7 noradrenergic cell groups. ERs were expressed with a clear rostrocaudal topography within the A1 and A2 populations, with 80–90% of noradrenergic neurons expressing ERα in the caudalmost medulla as compared with less than 5% rostral to the obex. Our findings demonstrate that, as in the rat, the ovine A1 and A2 neurons express ERs in a defined topographical manner, while, dissimilar to the rat, ERα is not synthesized by noradrenergic neurons in the other cell groups. These observations indicate that A1 and A2 noradrenergic neurons in the ovine brainstem are likely to be influenced by circulating estrogens and lay the neuroanatomical foundations for investigating the functional role of these cell populations within the gonadotropin-releasing hormone neuron network of the sheep.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Estrogen Receptor Expression in Brainstem Noradrenergic Neurons of the Sheep

et al. 1998

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“…These results thus raise the possibility that a noradrenergic system inhibits LH pulse amplitude in the ewe. Although more work is clearly needed to test this hypothesis, recent preliminary data [41] suggest that this system may play a role in the control of LH pulse amplitude in breeding season ewes.…”

Section: Lh Pulse Patternsmentioning

confidence: 99%

Is the Inhibitory Action of Estradiol on Luteinizing Hormone Pulse Frequency in Anestrous Ewes Mediated by Noradrenergic Neurons in the Preoptic Area?

Goodman

Robinson²,

Kendrick³

et al. 1995

Neuroendocrinology

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This study tested the hypothesis that estradiol inhibits luteinizing hormone (LH) pulse frequency in anestrous ewes by increasing the activity of an inhibitory noradrenergic (NE) system that acts in the ovine preoptic area (POA). The effects of estradiol on the release of NE and other neurotransmitters in thePOA were determined using intracranial microdialysis. Microdialysis probes (5 mm membrane length) were inserted via chronic guide tubes into the POA. Ringer’s solution was pumped through the probes at a rate of 2 µl/min for 8 h, the α-adrenergic antagonist phenoxybenzamine (PBZ; 60 µg/ml of Ringer’s solution) was then administered via the probe from hours 8 to 12, and Ringer’s solution alone was given the last 4 h. The outflow from the dialysis probes was collected every 20 min from 2 to 16 h and concentrations of aminergic transmitters and gamma aminobutyric acid determined by high-performance liquid chromatography. Blood samples were collected every 10 min throughout the experiment and the LH pulse patterns determined. Dialysis was done in the same neural area twice in each ewe, without (ovariectomy only) and with estadiol treatment (ovariectomy and a 1.5-cm-long Silastic capsule filled with crystalline estradiol placed subcutaneously for 2 days); the order of dialysis was randomized. As expected, estradiol decreased the LH pulse frequency. This negative feedback action of estradiol was associated with a decrease in mean NE concentrations in dialysate samples and an increase in the intra-animal variability of NE. Estradiol had no effect on any other neurotransmitter measured. Perfusion of PBZ through the dialysis probe increased NE levels, presumably by blocking adrenergic autoreceptors. However, this effect was only observed when the probes were located rostral to the decussation of the anterior commissure. Thus the autoregulatory control of NE release appears to vary in different hypothalamic areas. PBZ significantly increased the LH pulse amplitude, independently of any effects on NE release, raising the possibility that noradrenergic neurons act via α-adrenergic receptors to inhibit the LH pulse amplitude. In conclusion, these data demonstrate that estradiol decreases the mean NE levels in the POA of anestrous ewes, but may increase its episodic release.

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“…While the neurochemical identity of these neurons is not known, a variety of steroid-sensitive candidate systems have been identified (e.g. β-endorphin, γ-aminobutyric acid and norepinephrine [14, 18, 19, 20], and increased activation of steroid-receptive hypothalamic cells has been demonstrated in association with the LH surge [21, 22, 23]. …”

Section: Introductionmentioning

confidence: 99%

Progesterone Treatment That either Blocks or Augments the Estradiol-Induced Gonadotropin-Releasing Hormone Surge Is Associated with Different Patterns of Hypothalamic Neural Activation

Richter

Robinson²,

Evans³

2001

Neuroendocrinology

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Progesterone can either augment or inhibit the surge of gonadotropin-releasing hormone (GnRH) that drives the preovulatory luteinizing hormone (LH) surge. This study investigated the central mechanisms through which progesterone might achieve these divergent effects by examining the effects of exogenous steroids on the activation of GnRH neurons and non-GnRH-immunopositive cells in the preoptic area/anterior hypothalamus of steroid-treated ovariectomized ewes. Fos expression (an index of cellular activation) was examined during the estradiol-induced GnRH surge in ewes treated with progesterone using regimes that have been reported to either augment (progesterone pretreatment) or inhibit (progesterone treatment at the time of the surge-inducing estradiol increment) the GnRH surge. Control groups received either no progesterone pretreatment or no surge-inducing estradiol increment. Induction of an LH surge was associated with a significant (p < 0.0001) increase in the proportion of activated GnRH neurons, irrespective of whether ewes received progesterone pretreatment. However, the number of non-GnRH-immunopositive cells activated during the surge was significantly (p < 0.0001) increased in ewes that received the progesterone pretreatment. By contrast, the proportion of GnRH neurons and non-GnRH-immunopositive cells that expressed Fos was significantly (p < 0.0001) reduced in ewes in which the surge was inhibited by progesterone compared to ewes in which a surge was stimulated. These data indicate that (1) progesterone pretreatment increases the activation of non-GnRH cells during the estradiol-induced surge, but does not affect the proportion of GnRH neurons activated and (2) when administered concurrently with a surge-inducing estradiol increment, progesterone prevents the activation of GnRH neurons and non-GnRH cells that is normally associated with the estradiol-induced surge. Therefore, progesterone does not appear to augment the GnRH surge by increasing the proportion of GnRH neurons that are activated by estradiol, whereas inhibition of the GnRH surge involves prevention of the activation of GnRH neurons. Thus, the augmentation and inhibition of the GnRH surge by progesterone appear to be regulated via different effects on the GnRH neurosecretory system.

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Alpha Adrenergic Neurons Inhibit Luteinizing Hormone Pulse Amplitude in Breeding Season Ewes1

Cited by 16 publications

References 42 publications

Estrogen Receptor Expression in Brainstem Noradrenergic Neurons of the Sheep

Estrogen Receptor Expression in Brainstem Noradrenergic Neurons of the Sheep

Is the Inhibitory Action of Estradiol on Luteinizing Hormone Pulse Frequency in Anestrous Ewes Mediated by Noradrenergic Neurons in the Preoptic Area?

Progesterone Treatment That either Blocks or Augments the Estradiol-Induced Gonadotropin-Releasing Hormone Surge Is Associated with Different Patterns of Hypothalamic Neural Activation

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