Dopaminergic Neurones in the Zona incerta Exert a Stimulatory Control on Gonadotrophin Release via D&lt;sub&gt;1&lt;/sub&gt; Dopamine Receptors

James, Margaret D.; Mackenzie, F. J.; Tuohy-Jones, P.; Wilson, Catherine

doi:10.1159/000124758

Cited by 48 publications

(19 citation statements)

References 33 publications

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“…The complex effects of intracerebroventricular dopamine no doubt reflect multiple sites of dopamine action to modulate GnRH release. These include direct D1/D2 actions at GnRH neuron cell bodies, as shown here, D1-mediated effects in the zona incerta (9), and likely direct actions of dopamine on GnRH nerve terminals in the median eminence (32). The latter is the key site of action for dopamine's inhibitory influence on GnRH secretion in anestrous ewes (2).…”

Section: Discussionmentioning

confidence: 66%

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Liu

Herbison

2013

Endocrinology

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Numerous in vivo studies have shown that dopamine is involved in the regulation of LH secretion in mammals. However, the mechanisms through which this occurs are not known. In this study, we used green fluorescent protein-tagged GnRH neurons to examine whether and how dopamine may modulate the activity of adult GnRH neurons in the mouse. Bath-applied dopamine (10-80 M) potently inhibited the firing of approximately 50% of GnRH neurons. This resulted from direct postsynaptic inhibitory actions through D1-like, D2-like, or both receptors. Further, one third of GnRH neurons exhibited an increase in their basal firing rate after administration of SCH23390 (D1-like antagonist) and/or raclopride (D2-like antagonist) indicating tonic inhibition by endogenous dopamine in the brain slice. The role of dopamine in presynaptic modulation of the anteroventral periventricular nucleus (AVPV) ␥-aminobutyric acid/glutamate input to GnRH neurons was examined. Exogenous dopamine was found to presynaptically inhibit AVPV-evoked ␥-aminobutyric acid /glutamate postsynaptic currents in about 50% of GnRH neurons. These effects were, again, mediated by both D1-and D2-like receptors. Neither postsynaptic nor presynaptic actions of dopamine were found to be different between diestrous, proestrous, and estrous females, or males. Approximately 20% of GnRH neurons were shown to receive a dopaminergic input from AVPV neurons in male and female mice. Together, these observations show that dopamine is one of the most potent inhibitors of GnRH neuron excitability and that this is achieved through complex pre-and postsynaptic actions that each involve D1-and D2-like receptor activation. (Endocrinology 154: 340 -350, 2013)A lthough dopamine was among the first neurotransmitters investigated in relation to the control of the reproductive axis, there is little consensus regarding its effects on LH secretion or understanding of how it may impact upon GnRH neurons (1). Indeed, dopaminergic regulation of mammalian GnRH neurons is now something of a backwater and, with the exception of the A15 dopamine neuron influence on seasonality in sheep (2), there has been little progress in the field since the 1994 review by Kordon et al. (1).The lack of interest in the dopaminergic regulation of GnRH neurons is perhaps surprising given that the presence of tyrosine hydroxylase (TH)-immunoreactive terminals synapsing on GnRH neurons is one the most consistent ultrastructural features reported for GnRH neurons (3-5). Despite this evidence for direct dopaminergic inputs to GnRH neurons, the sites at which intracerebroventricular dopamine acts to modulate LH secretion in vivo, and the locations of dopaminergic inputs to GnRH neurons, are very unclear. For example, in rodents, dopamine appears to be able to act in the mediobasal hypothalamus and preoptic area, as well as zona incerta, to modulate LH secretion (6 -9).Studies in our laboratory have recently shown that a subpopulation of kisspeptin neurons located in the rostral periventricular area of the third ventric...

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Section: Discussionmentioning

confidence: 66%

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Liu

Herbison

2013

Endocrinology

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“…However, it is becoming obvious that there are a number of dopaminergic pathways which can influence gonadotrophins by either increasing or decreasing secretion. These include the A12, A14 and A15 dopaminergic cell groups with each pathway apparently modulating the LH pulse generator independently (18,(23)(24)(25). Non-specific approaches such as peripheral or intracerebroventricular (icv) injection of pharmacological agents may present conflicting signals to the LH pulse generator thus obscuring the individual input of each dopaminergic pathway.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of a Possible Role for the Dopamine D₁ and D₂ Receptors in the Steroid‐Dependent Suppression of Luteinizing Hormone Secretion in the Seasonally Anoestrous Ewe

Curlewis

Naylor

McNeilly

1991

J Neuroendocrinology

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This study was undertaken to determine whether dopaminergic suppression of pulsatile luteinizing hormone (LH) secretion during seasonal anoestrus in the ewe is mediated via the dopamine D, or D, receptor. This was tested by 1) assessing the response to dopamine D, and D, antagonists during seasonal anoestrus, and 2) determining the ability of D, and D, agonists to suppress pulsatile LH secretion during the breeding season. In seasonally anoestrous ewes the D, antagonist pirnozide increased LH pulse frequency although this effect did not reach significance (P=0.07). The D, antagonist SCH 23390 had no effect on LH pulse frequency. LH pulse amplitude and mean LH were not affected by either treatment. During the breeding season, ovariectomized oestradiol-implanted ewes were injected intracerebroventricularly with vehicle, LY 171555 (dopamine D, agonist) and SKF 38393 (D, agonist) with each drug tested at 50pg and 200pg. At the higher dose, LY 171555 significantly (P

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“…In general, this function is widely thought to be attributed to a cluster of dopaminergic neurons, known as the A13 incerto-hypothalamic neuronal group, that is confined to the medial ZI [52, 53, 55, 56]. Injections of dopamine or dopamine receptor type 1 (D 1 ) agonist into the medial ZI precipitate the preovulatory LH surge, whereas D 1 antagonists inhibit ovulation [54, 57]. In addition, preceding and during the preovulatory LH surge that occurs on the proestrus day or in ovariectomized rats primed with steroids, dopamine turnover is elevated in the medial ZI [15, 56].…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Glutamic Acid-Isoleucine May Induce Luteinizing Hormone Secretion via Multiple Pathways

Attademo

Rondini²,

Rodrigues

et al. 2006

Neuroendocrinology

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Neuropeptide glutamic acid-isoleucine (NEI) is a 14-amino acid peptide processed from prepro-melanin-concentrating hormone (ppMCH). In males, the localization of NEI is almost identical to that of MCH, the cell bodies of both being located primarily in the lateral hypothalamic area and zona incerta, projecting fibers throughout the brain. Although MCH has been widely studied, the role that NEI plays in brain circuitry has been poorly investigated. Recently, we showed that intracerebroventricular injection of NEI increases serum luteinizing hormone (LH) levels. In order to identify the anatomical substrate underlying this effect, we used combined immunohistochemistry methods to analyze the forebrains of females on the diestrus and proestrus days, as well as those of ovariectomized females treated with estradiol benzoate, with estradiol benzoate plus progesterone or with sesame oil (control animals). We found that ovariectomized females with no steroid treatment showed an increased number of NEI-immunoreactive neurons in the medial zona incerta. In addition, we observed dense to moderate NEI innervation of areas related to reproduction, including the organum vasculosum of the lamina terminalis, the anteroventral periventricular nucleus (AVPV) and the median eminence. The NEI fibers were in close apposition with the AVPV and gonadotropin-releasing hormone (GnRH) neurons expressing Fos in the afternoon of the proestrus day or following administration of estradiol benzoate plus progesterone. In the median eminence, NEI varicosities and terminal-like structures were in close proximity to blood vessels and GnRH fibers. Our results suggest that NEI might induce LH secretion in one of the following ways: by direct release into the median eminence, by modulation of GnRH neurons located in the preoptic area, by modulation of the GnRH terminals located in the median eminence or by an additive effect involving other neurotransmitters or neurohormones. Release of NEI might also induce LH secretion indirectly by modulating AVPV neurons.

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Dopaminergic Neurones in the Zona incerta Exert a Stimulatory Control on Gonadotrophin Release via D<sub>1</sub> Dopamine Receptors

Cited by 48 publications

References 33 publications

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Evaluation of a Possible Role for the Dopamine D₁ and D₂ Receptors in the Steroid‐Dependent Suppression of Luteinizing Hormone Secretion in the Seasonally Anoestrous Ewe

Neuropeptide Glutamic Acid-Isoleucine May Induce Luteinizing Hormone Secretion via Multiple Pathways

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Dopaminergic Neurones in the Zona incerta Exert a Stimulatory Control on Gonadotrophin Release via D<sub>1</sub> Dopamine Receptors

Cited by 48 publications

References 33 publications

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Dopamine Regulation of Gonadotropin-Releasing Hormone Neuron Excitability in Male and Female Mice

Evaluation of a Possible Role for the Dopamine D1 and D2 Receptors in the Steroid‐Dependent Suppression of Luteinizing Hormone Secretion in the Seasonally Anoestrous Ewe

Neuropeptide Glutamic Acid-Isoleucine May Induce Luteinizing Hormone Secretion via Multiple Pathways

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Evaluation of a Possible Role for the Dopamine D₁ and D₂ Receptors in the Steroid‐Dependent Suppression of Luteinizing Hormone Secretion in the Seasonally Anoestrous Ewe