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Journal articles on the topic 'Neurones à gonadoliberine [GnRH]'

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Published: 4 June 2021

Last updated: 13 February 2022

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1

Szlis, Michal, Jolanta Polkowska, and Anna Wójcik-Gładysz. "Can obestatin modulate the GnRH neurons activity?" Problems of Endocrinology 62, no. 5 (2016): 49–50. http://dx.doi.org/10.14341/probl201662549-50.

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Obestatin, an anorexigenic peptide acting at the central nervous system and on the periperial level, can co-create neuroendocrine network, which modulate the gonadotrophic axis activity. The aim of this study was to investigate the role of intracerebroventricular obestatin infusion on the activity of the gonadoliberine (GnRH) neurons activity.The experiment was performed on peripubertal Polish Merino sheep (n=24). Animals were divided into 2 groups: control (Ringer-Lock solution infusions; n=12) and experimental (obestatin infusion, 25μl/120μl/h; n=12). Infusions were performed over three consecutive days; blood samples were collected on day 0 and day 3. After the experiment, the animals were slaughtered, and the chosen brain tissue was preserved for IHC and Real Time RT-qPCR analysis.It was also shown that exogenous obestatin changes the selected gene expression of GnRH pulse generator, decreases the secretory activity of GnRH neurons, resulting from the inhibition of GnRH release from median eminence terminal nerves, and also decreases the GnRH receptor gene expression in pituitary. On the basis of the obtained results it can be concluded that obestatin may be involved in the modulation of reproduction processes in animals at the level of the central nervous system. However, the mechanism of its action requires further research, especially identifying the obestatin receptor itself.

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2

Shpakov, A. O., and K. V. Derkach. "Gonadoliberin – Synthesis, Secretion, Molecular Mechanisms and Targets of Action." Acta Biomedica Scientifica 4, no. 2 (2019): 7–15. http://dx.doi.org/10.29413/abs.2019-4.2.1.

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Decapeptide gonadoliberin (GnRH) is the most important regulator of the hypothalamic-pituitary-gonadal (HPG) axis that controls the synthesis and secretion of the luteinizing and follicle-stimulating hormones by gonadotrophs in the adenohypophysis. GnRH is produced by the specialized hypothalamic neurons using the site-specific proteolysis of the precursor protein and is secreted into the portal pituitary system, where it binds to the specific receptors. These receptors belong to the family of G protein-coupled receptors, and they are located on the surface of gonadotrophs and mediate the regulatory effects of GnRH on the gonadotropins production. The result of GnRH binding to them is the activation of phospholipase C and the calcium-dependent pathways, the stimulation of different forms of mitogen-activated protein kinases, as well as the activation of the enzyme adenylyl cyclase and the triggering of cAMP-dependent signaling pathways in the gonadotrophs. The gonadotropins, kisspeptin, sex steroid hormones, insulin, melatonin and a number of transcription factors have an important role in the regulation of GnRH1 gene expression, which encodes the GnRH precursor, as well as the synthesis and secretion of GnRH. The functional activity of GnRH-producing neurons depends on their migration to the hypothalamic region at the early stages of ontogenesis, which is controlled by anosmin, ephrins, and lactosamine-rich surface glycoconjugate. Dysregulation of the migration of GnRH-producing neurons and the impaired production and secretion of GnRH, lead to hypogonadotropic hypogonadism and other dysfunctions of the reproductive system. This review is devoted to the current state of the problem of regulating the synthesis and secretion of GnRH, the mechanisms of migration of hypothalamic GnRH-producing neurons at the early stages of brain development, the functional activity of the GnRH-producing neurons in the adult hypothalamus and the molecular mechanisms of GnRH action on the pituitary gonadotrophs. New experimental data are analyzed, which significantly change the current understanding of the functioning of GnRH-producing neurons and the secretion of GnRH, which is very important for the development of effective approaches for correcting the functions of the HPG axis.

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3

Robinson, Jane. "Prenatal programming of the female reproductive neuroendocrine system by androgens." Reproduction 132, no. 4 (2006): 539–47. http://dx.doi.org/10.1530/rep.1.00064.

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It has been clear for several decades that the areas of the brain that control reproductive function are sexually dimorphic and that the ‘programming actions’ of the male gonadal steroids are responsible for sex-specific release of the gonadotrophins from the pituitary gland. The administration of exogenous steroids to fetal/neonatal animals has pinpointed windows of time in an animals’ development when the reproductive neuroendocrine axis is responsive to the organisational influences of androgens. These ‘critical’ periods for sexual differentiation of the brain are trait- and species-specific. The neural network regulating the activity of the gonadotrophin releasing hormone (GnRH) neurones is vital to the control of reproductive function. It appears that early exposure to androgens does not influence the migratory pathway of the GnRH neurone from the olfactory placode or the size of the population of neurones that colonise the postnatal hypothalamus. However, androgens do influence the number and the nature of connections that these neurones make with other neural phenotypes. Gonadal steroid hormones play key roles in the regulation of GnRH release acting largely via steroid-sensitive intermediary neurones that impinge on the GnRH cells. Certain populations of hormonally responsive neurones have been identified that are sexually dimorphic and project from hypothalamic areas known to be involved in the regulation of GnRH release. These neurones are excellent candidates for the programming actions of male hormones in the reproductive neuroendocrine axis of the developing female.

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4

Constantin, S. "Physiology of the Gonadotrophin-Releasing Hormone (GnRH) Neurone: Studies from Embryonic GnRH Neurones." Journal of Neuroendocrinology 23, no. 6 (2011): 542–53. http://dx.doi.org/10.1111/j.1365-2826.2011.02130.x.

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5

Caligioni, C. S., C. Oliver, M. C. Jamur, and C. R. Franci. "Presence of Oxytocin Receptors in the Gonadotrophin-Releasing Hormone (GnRH) Neurones in Female Rats: A Possible Direct Action of Oxytocin on GnRH Neurones." Journal of Neuroendocrinology 19, no. 6 (2007): 439–48. http://dx.doi.org/10.1111/j.1365-2826.2007.01550.x.

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6

Barbotin, Anne-Laure, Vincent Prévot, and Paolo Giacobini. "Développement des neurones à GnRH dans le cerveau d’embryons humains." médecine/sciences 33, no. 4 (2017): 376–79. http://dx.doi.org/10.1051/medsci/20173304003.

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7

Vanacker, Charlotte, Sébastien G. Bouret, Paolo Giacobini, and Vincent Prévot. "Signalisation impliquant la neuropiline dans les neurones sécrétant la GnRH." médecine/sciences 37, no. 4 (2021): 366–71. http://dx.doi.org/10.1051/medsci/2021035.

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La survie d’une espèce dépend de deux processus intimement liés : la reproduction, d’une part, et l’équilibre entre les besoins énergétiques et l’approvisionnement en sources d’énergie par l’alimentation, d’autre part. Ces deux processus sont contrôlés dans le cerveau par l’hypothalamus, qui produit des neurohormones agissant sur l’hypophyse pour piloter diverses fonctions physiologiques. L’une de ces neurohormones, la GnRH, contrôle non seulement la maturation et le fonctionnement des organes reproducteurs, incluant les ovaires et les testicules, lors de la puberté et à l’âge adulte, mais aussi l’attirance sexuelle. De récentes découvertes suggèrent que la signalisation impliquant la neuropiline-1 dans les neurones sécrétant la GnRH jouerait un rôle charnière dans la coordination du neurodéveloppement et des adaptations physiologiques et comportementales nécessaires au déclenchement de la puberté et à l’acquisition de la fonction de reproduction. Dans cet article de synthèse, nous replaçons ces découvertes dans le contexte de récents travaux montrant que les voies de signalisation des sémaphorines de classe 3 sont impliquées dans la physiopathologie non seulement de l’infertilité, mais aussi de l’obésité. Nous discutons également l’implication potentielle des neurones produisant la GnRH dans la perception des odeurs sociales et dans la précocité de la maturation sexuelle. L’hypothèse selon laquelle l’activité de ces neurones au cours du développement postnatal constituerait le chaînon manquant entre la prise de poids, le déclenchement de la puberté et le comportement sexuel, ouvre la voie à une meilleure compréhension de l’implication de l’homéostasie énergétique dans la maturation sexuelle, et pourrait aussi avoir des implications thérapeutiques pour la puberté précoce.

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8

Park, S.-K., D. A. Strouse, and M. Selmanoff. "Prolactin- and testosterone-induced inhibition of LH secretion after orchidectomy: role of catecholaminergic neurones terminating in the diagonal band of Broca, medial preoptic nucleus and median eminence." Journal of Endocrinology 148, no. 2 (1996): 291–301. http://dx.doi.org/10.1677/joe.0.1480291.

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Abstract Central catecholaminergic neurones projecting to specific hypothalamic structures are involved in stimulating and inhibiting the activity of the GnRH-containing neurosecretory neurones. Both testosterone and elevated circulating prolactin (PRL) levels inhibit postcastration LH release. Three groups of adult male rats were orchidectomized and adrenalectomized, received corticosterone replacement and were: (i) administered purified ovine PRL (oPRL; 2400 μg/s.c. injection) or (ii) its diluent, polyvinylpyrrolidone (PVP), every 12 h, or (iii) received physiological testosterone replacement for 2 days. At 0, 2 and 6 days postcastration, norepinephrine (NE), epinephrine (E) and dopamine (DA) turnover were estimated by the α-methyl-p-tyrosine method in three micro-dissected hypothalamic structures: the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis (DBB(ovlt)), the medial preoptic nucleus (MPN) and the median eminence (ME). In control (PVP-treated) rats, serum LH concentrations increased eightfold at 2 and 6 days postcastration and this rise was prevented by testosterone. oPRL treatment transiently suppressed LH secretion at 2 but not 6 days postcastration. Castration significantly decreased basal rat PRL (rPRL) levels at 2 and 6 days and testosterone administration partially prevented this effect. NE turnover in the ME and E turnover in the MPN increased markedly at 2 and 6 days postcastration, and testosterone replacement for 2 days prevented these increases. Thus, noradrenergic neurones innervating the ME and adrenergic neurones innvervating the MPN may drive postcastration LH secretion by providing stimulatory afferent input to the GnRH neurones. It was striking to observe that oPRL blocked the increases in both ME NE and MPN E turnover at 2 but not 6 days postcastration. Hence, oPRL may transiently suppress LH release by an inhibitory action on these NE and E neurones. DA turnover in the DBB(ovlt) was significantly decreased by 6 days postcastration. Testosterone-treated (2 days postcastration) and oPRL-treated (2 and 6 days postcastration) rats exhibited turnover values indistinguishable from day 0 controls. Hence, the A14 dopaminergic neurones, which synapse on GnRH neurones in the rostral preoptic area and may exert an inhibitory effect on them, are positively regulated by PRL and perhaps by testosterone as well. Autoregulatory feedback suppression of endogenous rPRL secretion by oPRL was observed both 2 and 6 days postcastration. In contrast to the A14 dopaminergic neurones, turnover in the A12 tuberoinfundibular dopaminergic (TIDA) neurones innervating the ME increased significantly by 6 days postcastration in control rats while oPRL administration further increased ME DA turnover at both 2 and 6 days. Hence, autofeedback regulation of rPRL secretion persists through at least 6 days of oPRL exposure temporally associated with markedly increased turnover in the TIDA neurones. In summary, our results support the hypothesis that the inhibitory effect of PRL on postcastration LH release is mediated by suppression of the activity of NE neurones innervating the ME and E neurones terminating in the MPN which, with time, become refractory to continued PRL exposure. Journal of Endocrinology (1996) 148, 291–301

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9

Han, S. K., K. Lee, J. P. Bhattarai, and A. E. Herbison. "Gonadotrophin-Releasing Hormone (GnRH) Exerts Stimulatory Effects on GnRH Neurones in Intact Adult Male and Female Mice." Journal of Neuroendocrinology 22, no. 3 (2010): 188–95. http://dx.doi.org/10.1111/j.1365-2826.2009.01950.x.

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10

Smith, M. "Neural signals that regulate GnRH neurones directly during the oestrous cycle." Reproduction 122, no. 1 (2001): 1–10. http://dx.doi.org/10.1530/reprod/122.1.1.

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11

Urbanski, H. "Mechanisms mediating the response of GnRH neurones to excitatory amino acids." Reviews of Reproduction 1, no. 3 (1996): 173–81. http://dx.doi.org/10.1530/revreprod/1.3.173.

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12

Urbanski, H. "Mechanisms mediating the response of GnRH neurones to excitatory amino acids." Reviews of Reproduction 1, no. 3 (1996): 173–81. http://dx.doi.org/10.1530/ror.0.0010173.

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13

Bowe, J., X. F. Li, D. Sugden, J. A. Katzenellenbogen, B. S. Katzenellenbogen, and K. T. O'Byrne. "The Effects of the Phytoestrogen, Coumestrol, on Gonadotropin-Releasing Hormone (GnRH) mRNA Expression in GT1-7 GnRH Neurones." Journal of Neuroendocrinology 15, no. 2 (2003): 105–8. http://dx.doi.org/10.1046/j.1365-2826.2003.00991.x.

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14

Hajdú, P., T. Ikemoto, Y. Akazome, M. K. Park, and Y. Oka. "Terminal Nerve Gonadotrophin-Releasing Hormone (GnRH) Neurones Express Multiple GnRH Receptors in a Teleost, the Dwarf Gourami (Colisa lalia)." Journal of Neuroendocrinology 19, no. 6 (2007): 475–79. http://dx.doi.org/10.1111/j.1365-2826.2007.01553.x.

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15

Abraham, E., O. Palevitch, S. Ijiri, S. J. Du, Y. Gothilf, and Y. Zohar. "Early Development of Forebrain Gonadotrophin-Releasing Hormone (GnRH) Neurones and the Role of GnRH as an Autocrine Migration Factor." Journal of Neuroendocrinology 20, no. 3 (2008): 394–405. http://dx.doi.org/10.1111/j.1365-2826.2008.01654.x.

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16

Ozcan, Mete, Ergul Alcin, Ahmet Ayar, Bayram Yılmaz, Suleyman Sandal, and Haluk Kelestimur. "Kisspeptin-10 elicits triphasic cytosolic calcium responses in immortalized GT1-7 GnRH neurones." Neuroscience Letters 492, no. 1 (2011): 55–58. http://dx.doi.org/10.1016/j.neulet.2011.01.054.

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17

MIGAUD, M., H. DARDENTE, M. KELLER, M. BATAILLER, M. MEURISSE, and D. PILLON. "Contrôle neuroendocrinien de la reproduction chez les mammifères." INRA Productions Animales 29, no. 4 (2019): 255–66. http://dx.doi.org/10.20870/productions-animales.2016.29.4.2967.

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La reproduction recouvre l’ensemble des processus biologiques qui permettent d’assurer la survie d’une espèce grâce à la naissance de nouveaux individus. Cette propriété fondamentale et obligatoire du monde vivant repose sur un mécanisme efficace et extrêmement complexe. Chez les vertébrés, c’est l’axe hypothalamo-hypophyso-gonadique qui est le cadre anatomique responsable de la compétence reproductive et donc de la pérennité des espèces. La coordination de ce système biologique à trois étages repose sur le contrôle neuronal de libération de la « Gonadotrophin Releasing Hormone » (GnRH), système localisé dans la partie rostrale de l’hypothalamus. La libération de GnRH dans le système porte hypothalamo-hypophysaire stimule la sécrétion des gonadotropines hypophysaires qui sont impliquées dans le déclenchement de la puberté et la régulation de la fonction de reproduction. Cette revue fournit des éléments de compréhension sur le fonctionnement du contrôle neuroendocrine de l’axe hypothalamo-hypophyso-gonadique chez les mammifères, en particulier, sur les propriétés du système à GnRH, le contrôle neuroendocrinien des cycles ovariens, l’effet de neuropeptides hypothalamiques «kisspeptin » sur les neurones à GnRH, le déclenchement de la puberté, la saisonnalité et conclue sur les perspectives de recherche dans cette discipline de la neurobiologie.

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18

Tiwary, Basant K., R. Kirubagaran, and Arun K. Ray. "Gonadotropin releasing hormone (GnRH) neurones of triploid catfish, Heteropneustes fossilis (Bloch): an immunocytochemical study." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 132, no. 2 (2002): 375–80. http://dx.doi.org/10.1016/s1095-6433(02)00037-5.

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19

Kalló, I., B. Vida, L. Deli, et al. "Co-Localisation of Kisspeptin with Galanin or Neurokinin B in Afferents to Mouse GnRH Neurones." Journal of Neuroendocrinology 24, no. 3 (2012): 464–76. http://dx.doi.org/10.1111/j.1365-2826.2011.02262.x.

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20

Tillet, Yves, Sophie Picard, and Isabelle Franceschini. "Les neuropeptides hypothalamiques dans le contrôle des neurones à GnRH. Étude neuroanatomique chez la brebis." Journal de la Société de Biologie 203, no. 1 (2009): 19–28. http://dx.doi.org/10.1051/jbio:2009003.

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21

Thiery, JC, and GB Martin. "Neurophysiological control of the secretion of gonadotrophin-releasing hormone and luteinizing hormone in the sheep--a review." Reproduction, Fertility and Development 3, no. 2 (1991): 137. http://dx.doi.org/10.1071/rd9910137.

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The anterior pituitary gland secretes pulses of luteinizing hormone (LH) in response to pulses of gonadotrophin-releasing hormone (GnRH) released into the hypophysial portal blood by the hypothalamus. The pulsatile nature of the secretions is very important because the frequency of the pulses is directly related to the activity of the GnRH neurons. We can therefore take advantage of this phenomenon to develop mechanistic interpretations of responses to experimental treatments designed to unravel the neural pathways that influence what is, arguably, the most important individual signal controlling the activity of the reproductive system. We might also resolve the disagreements in the literature covering the neuropharmacology of gonadotrophin secretion. In this review, we describe work towards this end in the sheep. Most (95%) of the 2500 GnRH cell bodies in the sheep brain are located in a region covering the anterior hypothalamus, the medial preoptic area, the diagonal band of Broca, and the septum. The axons of up to 50% of these cells terminate in the organum vasculosum of the lamina terminalis. The remainder terminate in the median eminence and form the final common pathway for the many factors that affect gonadotrophin secretion. Among the factors known to affect the frequency of the pulses (or the activity of the GnRH neurons) are nutrition, pheromones, photoperiod and gonadal steroids (negative and positive feedback). Factors that affect GnRH pulse amplitude are more difficult to determine because variations in pituitary responsiveness prevent the use of LH patterns as a 'bioassay'. Techniques developed recently have allowed the direct measurement of GnRH pulse amplitude and revealed inhibitory effects of oestradiol, but we do not know whether this effect is due to a reduction in the amount of GnRH released by each neurone or a reduction in the number of neurones releasing a pulse. It is unlikely that the factors that alter pulse frequency do so by directly affecting the GnRH cells. For example, it is obvious that other cells, with specific receptors for pheromonal or nutritional stimuli, formulate a signal that is transferred to the GnRH cells via interneurones. Similarly, it is likely that a hypothalamic clock intervenes between photoperiodic inputs and GnRH output. Opioidergic neurons have been proposed as a link in this system, but the complexity of their action makes it unlikely that they directly affect the GnRH neurons. The responses to steroids are simple and rapid, but steroid receptors have not been found in GnRH cells, so at least one other set of interneurones is involved.(ABSTRACT TRUNCATED AT 400 WORDS)

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22

Tata, B., Z. Csaba, S. Jacquier, and N. De Roux. "La Rabconnectin-3 ? est une protéine synaptique nécessaire à l’activation et la maturation postnatale des neurones GnRH." Annales d'Endocrinologie 76, no. 4 (2015): 352. http://dx.doi.org/10.1016/j.ando.2015.07.166.

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23

Tillet, Yves, Sébastien Tourlet, Sophie Picard, Pierre-Yves Sizaret, and Alain Caraty. "Morphofunctional interactions between galanin and GnRH-containing neurones in the diencephalon of the ewe. The effect of oestradiol." Journal of Chemical Neuroanatomy 43, no. 1 (2012): 14–19. http://dx.doi.org/10.1016/j.jchemneu.2011.09.005.

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24

Grigoryan, O. R., A. A. Okhotnikova, and E. N. Andreeva. "Hypothalomo-pituitary-gonadal axis in girls with type 1 diabetes mellitus menstrual disorders and ovarian dysfunction." Problems of Endocrinology 55, no. 5 (2009): 38–43. http://dx.doi.org/10.14341/probl200955538-43.

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Type 1 diabetes mellitus (DM) has negative effect on the development and functioning of the reproductive system in young girls. The time of onset of type 1 DM (especially in the puberty period), duration of the disease, and poor compensation of disturbed carbohydrate metabolism are supposed to be the most probable causes of delayed pubertal development exerting negative effect on the age of menarche and increasing the frequency of menstrual problems (largely oligo- and amenorrhea). Despite a wealth of relevant investigations, the cause of reproductive dysfunction remains unknown even though negative effect of type 1 DM on different components of the hypothalamo-pituitary-ovarian axis has been fairly well documented. The pathogenetic mechanisms of reproductive disorders may consist of suppression of pulsed production of gonadotropin releasing hormone (GnRH) due to enhanced central dopaminergic and opiate activities, decreased concentration of insulin receptors on GnRH-synthesizing neurones, and changes of serum leptin level in the affected girls. In patients with type 1 DM, hypothalamic effects on the pituitary may be supplemented by the direct action of products of free radical oxidative activity leading to a decrease in the production of trophic hormones. Also considered, is primary ovarian origin of menstrual disturbances in girls with type 1 DM. Of great importance are studies concerning autoantibodies against different ovarian structures, variations in concentrations of insulin-like growth factor-1 (IGF-1) and hormone ghrelin.

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25

Merkley, C. M., L. M. Coolen, R. L. Goodman, and M. N. Lehman. "Evidence for Changes in Numbers of Synaptic Inputs onto KNDy and GnRH Neurones during the Preovulatory LH Surge in the Ewe." Journal of Neuroendocrinology 27, no. 7 (2015): 624–35. http://dx.doi.org/10.1111/jne.12293.

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26

Graham, G. K., T. Boswell, Q. Li, et al. "280. Photo inhibited heat shock protein 108 gene expression in the chicken hypothalamus." Reproduction, Fertility and Development 17, no. 9 (2005): 117. http://dx.doi.org/10.1071/srb05abs280.

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In domestic juvenile chickens kept on short days, photoinduced luteinsing hormone (LH) release, and by inference gonadotrophin-releasing hormone (GnRH) release, are readily detectable within 4 days of photostimulation.2 The molecular mechanisms responsible for the rapid photoinduced release of LH and GnRH in avian species are unknown. It has been suggested that it might involve a cascade of gene expression associated with an increase in cfos in the basal hypothalamus and glial cells in the median eminence.1 A microarray was made consisting of known genes of interest and clones obtained from a hypothalamic short day/long day subtractive library. An experiment was undertaken to determine if this reproductive neuroendocrine microarray could detect new targets for study in the chicken model of photostimulated GnRH release. The microarray was interrogated with hypothalamic RNA from juvenile chickens showing an increase in plasma LH after 4 days of photostimulation. Six genes were identified as showing changes in expression after photostimulation on the microarray. However, only one gene, encoding heat shock protein 108 (HSP108), could be confirmed by quantitative competitive RT-PCR. The expression of this gene decreased both in the hypothalamus and the optic tectum. Treatment of short day juvenile chickens with thyroxine, to mimic the effects of photostimulation, resulted in LH release and depression of HSP108 expression in the anterior but not the basal hypothalamus. Immunocytochemical analyses showed that HSP108 is widely distributed in the brain including glial-like cells with terminals in the median eminence. HSP108 is suggested as a candidate protein involved in the regulation of gonadotrophin release from the median eminence by glial cells. (1)Meddle SL and Follett BK (1995) Photoperiodic activation of fos-like immunoreactive protein in neurones within the tuberal hypothalamus of Japanese quail. Journal of Comparative Physiology [A] 176(1), 79–89.(2)Sreekumar KP and Sharp PJ (1998) Ontogeny of the photoperiodic control of prolactin and luteinizing hormone secretion in male and female bantams (Gallus domesticus). General and Comparative Endocrinology 109(1), 69–74.

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27

Egginger, Johann-Günther, Caroline Parmentier, Ghislaine Garrel, et al. "Direct Evidence for the Co-Expression of URP and GnRH in a Sub-Population of Rat Hypothalamic Neurones: Anatomical and Functional Correlation." PLoS ONE 6, no. 10 (2011): e26611. http://dx.doi.org/10.1371/journal.pone.0026611.

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28

Agça, Esma, Martine Batailler, Yves Tillet, Philippe Chemineau, and Anne H. Duittoz. "Modulation of estrogen receptors during development inhibits neurogenesis of precursors to GnRH-1 neurones: In vitro studies with explants of ovine olfactory placode." Brain Research 1223 (August 2008): 34–41. http://dx.doi.org/10.1016/j.brainres.2008.05.026.

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29

GUILLAUME, D. "Action de la photopériode sur la reproduction des équidés." INRAE Productions Animales 9, no. 1 (2020): 61–69. http://dx.doi.org/10.20870/productions-animales.1996.9.1.4035.

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Juments et étalons présentent une phase de reproduction pendant les jours croissants ou longs, au printemps et en été. La majorité des juments n’ont pas d’ovulation en hiver. Ce rythme annuel de reproduction est synchronisé par les variations annuelles de la longueur du jour. Un éclairement artificiel de 14,5 h, débuté en hiver, avance la première ovulation annuelle des juments. Certaines des étapes de la transmission de l’information lumineuse ont été vérifiées chez les équidés. Le message lumineux est transformé en influx nerveux par des cellules spécialisées de la rétine. Cet influx, via le noyau supra-chiasmatique puis le ganglion cervical supérieur, agit sur la glande pinéale. Les pinéalocytes répondent à une stimulation noradrénergique en libérant la mélatonine. Cette hormone, sécrétée pendant la phase obscure, agit sur des récepteurs membranaires spécifiques. L’administration de mélatonine exogène sous forme d’implants sous-cutanés ou, dans certaines conditions, sous forme orale, supprime l’effet photostimulant d’un jour long. L’utilisation d’implants est actuellement à l’étude pour mettre au point un traitement de désaisonnement. La sécrétion des neurones à GnRH est ensuite régulée par des neuromédiateurs. La naloxone, antagoniste des opiacées endogènes, induit une décharge de GnRH suivie d’une libération de LH et de FSH chez la jument en inactivité. Les hormones thyroïdiennes ont probablement une action à ce niveau. L’alternance d’un mois de jours courts et d’un mois de jours longs qui permet, chez les petits ruminants mâles, d’abolir les variations saisonnières est, dans l’état actuel des travaux, inefficace chez l’étalon ou la jument. Pour avancer la date de la première ovulation annuelle, les éleveurs ne disposent actuellement que d’un traitement comportant 14,5 h d’éclairement par jour, commencé vers le solstice d’hiver et appliqué pendant 35 jours.

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Cobellis, Vallarino, Meccariello, et al. "Fos Localization in Cytosolic and Nuclear Compartments in Neurones of the Frog, Rana esculenta, Brain: An Analysis Carried Out in Parallel with GnRH Molecular Forms." Journal of Neuroendocrinology 11, no. 9 (2001): 725–35. http://dx.doi.org/10.1046/j.1365-2826.1999.00390.x.

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Sirinathsinghji, D. J. S., M. Motta, and L. Martini. "Induction of precocious puberty in the female rat after chronic naloxone administration during the neonatal period: the opiate 'brake' on prepubertal gonadotrophin secretion." Journal of Endocrinology 104, no. 2 (1985): 299–307. http://dx.doi.org/10.1677/joe.0.1040299.

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ABSTRACT Studies were undertaken using the opiate receptor antagonist naloxone to examine the hypothesis that endogenous opiates may have a restraining effect on prepubertal gonadotrophin secretion and may be involved in the maturation of the central nervous system mechanisms regulating the onset of puberty in the female rat. Naloxone (2·5 mg/kg) administered intraperitoneally every 6 h to female rats from day 1 to day 10 of postnatal life significantly (P <0·001) advanced the age of onset of puberty assessed in terms of the day of vaginal opening and first oestrus (32·3 ± 0·2 vs 40·8 ± 0·4 days in control saline-treated animals). Animals so treated with naloxone showed significantly (P < 0·001) higher levels of FSH (761·4 ± 87·6 vs 483·8± 57·2 μg/l in control animals) and LH (562·8 ± 57·4 vs 351·3 ± 43·3 μg/l in control animals) at the first late pro-oestrus and a significantly (P < 0·001) higher number of ova released at first oestrus (12·4 ± 0·4 vs 8·1±0·3 in controls). Body weight at first oestrus was significantly (P <0·001) lower in the naloxone-treated animals, an indication that these animals were much younger. The weights (per 100 g body wt) of the ovaries and uteri at the first oestrus were significantly (P <0·01) higher in the naloxone-treated rats than in the controls. However, there were no significant differences in the weights of the adrenals and anterior pituitary glands between the two groups of animals. A study of the cyclic patterns of the neonatally naloxone-treated animals performed for 15 consecutive cycles after the first oestrus showed normal 4- or 5-day cycles similar to those occurring in the saline-treated animals. The lengths of the first and second cycles in the naloxone-treated animals were not significantly different from controls. No significant differences in body weight or in organ weights at oestrus or in the levels of LH and FSH determined during the various stages of the oestrous cycle were found between naloxone- and saline-treated animals when these parameters were examined at 3 months of age. Naloxone had no effect on onset of puberty when administered during the other stages of prepubertal life. The mechanisms by which naloxone acts specifically during the neonatal period to induce precocious puberty are at present not known but are being investigated; they may be related to naloxone-induced alterations in the inhibitory synaptic arrangements between opiatergic and gonadotrophin-releasing hormone (GnRH) neurones, with a resulting decrease in the inhibitory influence exerted by endogenous opioids on GnRH neurones during this period of intense neurological development. The results suggest that the endogenous opiate peptides could play a key role in the central mechanisms which trigger the onset of puberty in the female rat. J. Endocr. (1985) 104, 299–307

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Prevot, Bouret, Croix та ін. "Evidence That Members of the TGFβ Superfamily Play a Role in Regulation of the GnRH Neuroendocrine Axis: Expression of a Type I Serine-Threonine Kinase Receptor for TGRβ and Activin in GnRH Neurones and Hypothalamic Areas of the Female Rat". Journal of Neuroendocrinology 12, № 7 (2001): 665–70. http://dx.doi.org/10.1046/j.1365-2826.2000.00508.x.

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Fergani, C., J. E. Routly, D. N. Jones, L. C. Pickavance, R. F. Smith, and H. Dobson. "KNDy neurone activation prior to the LH surge of the ewe is disrupted by LPS." Reproduction 154, no. 3 (2017): 281–92. http://dx.doi.org/10.1530/rep-17-0191.

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In the ewe, steroid hormones act on the hypothalamic arcuate nucleus (ARC) to initiate the GnRH/LH surge. Within the ARC, steroid signal transduction may be mediated by estrogen receptive dopamine-, β-endorphin- or neuropeptide Y (NPY)-expressing cells, as well as those co-localising kisspeptin, neurokinin B (NKB) and dynorphin (termed KNDy). We investigated the time during the follicular phase when these cells become activated (i.e., co-localise c-Fos) relative to the timing of the LH surge onset and may therefore be involved in the surge generating mechanism. Furthermore, we aimed to elucidate whether these activation patterns are altered after lipopolysaccharide (LPS) administration, which is known to inhibit the LH surge. Follicular phases of ewes were synchronised by progesterone withdrawal and blood samples were collected every 2 h. Hypothalamic tissue was retrieved at various times during the follicular phase with or without the administration of LPS (100 ng/kg). The percentage of activated dopamine cells decreased before the onset of sexual behaviour, whereas activation of β-endorphin decreased and NPY activation tended to increase during the LH surge. These patterns were not disturbed by LPS administration. Maximal co-expression of c-Fos in dynorphin immunoreactive neurons was observed earlier during the follicular phase, compared to kisspeptin and NKB, which were maximally activated during the surge. This indicates a distinct role for ARC dynorphin in the LH surge generation mechanism. Acute LPS decreased the percentage of activated dynorphin and kisspeptin immunoreactive cells. Thus, in the ovary-intact ewe, KNDy neurones are activated prior to the LH surge onset and this pattern is inhibited by the administration of LPS.

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Tortonese, D. J., and G. A. Lincoln. "Effects of melatonin in the mediobasal hypothalamus on the secretion of gonadotrophins in sheep: role of dopaminergic pathways." Journal of Endocrinology 146, no. 3 (1995): 543–52. http://dx.doi.org/10.1677/joe.0.1460543.

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Abstract Previous studies have shown that treatment with microimplants of melatonin in the mediobasal hypothalamus (MBH) of sexually inactive Soay rams exposed to long days induces an increase in the secretion of FSH and reactivation of the testicular axis, as normally occurs in response to short days. The current study was conducted to investigate the possible involvement of hypothalamic dopaminergic (DA) systems in this melatonin-induced effect. At 10 weeks under long days, sexually inactive Soay rams were treated in the MBH with micro-implants containing bromocriptine (DA agonist) or sulpiride (DA antagonist), given alone or in combination with melatonin, to establish whether the DA drugs would mimic or negate the effects of melatonin. All micro-implants were inserted bilaterally and left in place for 14 weeks; the study lasted a total of 28 weeks (14 weeks implant period and 14 weeks post-implant period) while the animals remained under long days. The ability of the micro-implants to release bromocriptine and sulpiride for 14 weeks was confirmed by incubating implants in vitro and testing for the presence of the compounds in the incubate using a pituitary cell bioassay. Profiles of FSH, determined in blood samples collected three times weekly, were significantly different among treatments (time × treatment interaction, P<0·001, ANOVA). Melatonin in the MBH induced a marked increase in the concentrations of FSH during the implant period, and a decrease during the post-implant period (P<0·001). Bromocriptine given alone in the MBH induced a decrease in the concentrations of FSH which became statistically different from the control during the post-implant period (P<0·05). Treatment with sulpiride alone also resulted in a suppressive effect during the post-implant period (P<0·01). When given in combination with melatonin, bromocriptine or sulpiride significantly reduced the melatonin-induced increase in the concentrations of FSH observed during the implant period (P<0·001). The results support the view that DA pathways in the MBH play an important role in the inhibitory regulation of gonadotrophin secretion in the ram. The inhibitory effect of bromocriptine is likely to result from the direct activation of the hypothalamic DA receptors linked to GnRH neurones regulating the secretion of FSH. The apparent paradoxical inhibitory effect of sulpiride is thought to be due to enhanced gonadal steroid negative feedback resulting from blockade of the inhibitory DA pathways, as evidenced by significantly increased secretion of testosterone (P<0·05) in the animals receiving sulpiride in combination with melatonin. The observation that DA drugs modified the effects of melatonin in the MBH provides evidence that hypothalamic DA pathways may participate in the mechanism by which melatonin mediates the effects of photoperiod on reproductive function in the ram. Journal of Endocrinology (1995) 146, 543–552

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Smith, MJ, and L. Jennes. "Neural signals that regulate GnRH neurones directly during the oestrous cycle." Reproduction, July 1, 2001, 1–10. http://dx.doi.org/10.1530/rep.0.1220001.

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GnRH, produced by a loose network of neurones in the basal forebrain, is the primary brain signal responsible for the release of LH and FSH from the anterior pituitary gland. The ovarian steroid hormone oestradiol feeds back at both the central nervous system and the anterior pituitary to regulate the patterns of release of GnRH and the gonadotrophins. Although recent evidence indicates that oestradiol may act directly on some GnRH neurones through classical genomic mechanisms, data from published studies have demonstrated that neurotransmission of afferent neuronal systems that are receptive to oestradiol is necessary to drive reproductive cyclicity. Many classical neurotransmitters and neuropeptides alter GnRH neuronal activity, through direct and sometimes indirect actions. This review focuses on the neurotransmitters that regulate GnRH neurones by binding to and activating specific membrane receptors that are expressed in GnRH neurones. These include the catecholamines, gamma-aminobutyric acid, glutamate, neuropeptide Y, neurotensin, beta-endorphin and vasoactive intestinal polypeptide. On the basis of recent molecular and neuroanatomical evidence, it is proposed that oestradiol influences the activity of these neurotransmitter and neuropeptide systems within the GnRH network to drive reproductive cyclicity.

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Duittoz, AH, and M. Batailler. "Pulsatile GnRH secretion from primary cultures of sheep olfactory placode explants." Reproduction, November 1, 2000, 391–96. http://dx.doi.org/10.1530/reprod/120.2.391.

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The aim of this study was to investigate the development of pulsatile GnRH secretion by GnRH neurones in primary cultures of olfactory placodes from ovine embryos. Culture medium was collected every 10 min for 8 h to detect pulsatile secretion. In the first experiment, pulsatile secretion was studied in two different sets of cultures after 17 and 24 days in vitro. In the second experiment, a set of cultures was tested after 10, 17 and 24 days in vitro to investigate the development of pulsatile GnRH secretion in each individual culture. This study demonstrated that (i) primary cultures of GnRH neurones from olfactory explants secreted GnRH in a pulsatile manner and that the frequency and mean interpulse duration were similar to those reported in castrated ewes, and (ii) pulsatile secretion was not present at the beginning of the culture but was observed between 17 and 24 days in vitro, indicating the maturation of individual neurones and the development of their synchronization.

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Dobson, H., S. Ghuman, S. Prabhakar, and R. Smith. "A conceptual model of the influence of stress on female reproduction." Reproduction, February 1, 2003, 151–63. http://dx.doi.org/10.1530/rep.0.1250151.

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Intriguingly, similar neurotransmitters and nuclei within the hypothalamus control stress and reproduction. GnRH neurone recruitment and activity is regulated by a balance between stimulation, suppression and permissiveness controlled by noradrenaline, neuropeptide Y and serotonin from the brain stem, impact from glutamate in the medial preoptic area and neuropeptide Y in the arcuate nucleus, in opposition to the restraining influences of gamma-aminobenzoic acid within the medial preoptic area and opioids from the arcuate nucleus. Stress also activates neuropeptide Y perikarya in the arcuate nucleus and brain stem noradrenaline neurones. The latter project either indirectly, via the medial preoptic area, or directly to the paraventricular nucleus to release corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP). Within the medial preoptic area, GnRH neurones synapse with CRH and AVP axons. Stimulation of CRH neurones in the paraventricular nucleus also activates gamma-aminobenzoic acid and opioid neurones in the medial preoptic area and reduces GnRH cell recruitment, thereby decreasing GnRH pulse frequency. Oestradiol enhances stress-induced noradrenaline suppression of LH pulse frequency but when applied in the paraventricular nucleus or brain stem, and not in the medial preoptic area or arcuate nucleus. The importance of CRH and AVP in the medial preoptic area needs confirming in a species other than the rat, which uses adrenal activation to time the onset of the GnRH surge. Another stress-activated pathway involves the amygdala and bed of the nucleus stria terminalis, which contain CRH neurones and accumulate gamma-aminobenzoic acid during stress.

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"Editorial Comment: Might Oestrogen Act Directly on GnRH Neurones?" Journal of Neuroendocrinology 11, no. 5 (1999): 323–24. http://dx.doi.org/10.1046/j.1365-2826.1999.00349.x.

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Berland, Marco, Luis Paiva, Lig Alondra Santander, and Marcelo Héctor Ratto. "Distribution of GnRH and Kisspeptin Immunoreactivity in the Female Llama Hypothalamus." Frontiers in Veterinary Science 7 (February 2, 2021). http://dx.doi.org/10.3389/fvets.2020.597921.

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Llamas are induced non-reflex ovulators, which ovulate in response to the hormonal stimulus of the male protein beta-nerve growth factor (β-NGF) that is present in the seminal plasma; this response is dependent on the preovulatory gonadotrophin-releasing hormone (GnRH) release from the hypothalamus. GnRH neurones are vital for reproduction, as these provide the input that controls the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland. However, in spontaneous ovulators, the activity of GnRH cells is regulated by kisspeptin neurones that relay the oestrogen signal arising from the periphery. Here, we investigated the organisation of GnRH and kisspeptin systems in the hypothalamus of receptive adult female llamas. We found that GnRH cells exhibiting different shapes were distributed throughout the ventral forebrain and some of these were located in proximity to blood vessels; sections of the mediobasal hypothalamus (MBH) displayed the highest number of cells. GnRH fibres were observed in both the organum vasculosum laminae terminalis (OVLT) and median eminence (ME). We also detected abundant kisspeptin fibres in the MBH and ME; kisspeptin cells were found in the arcuate nucleus (ARC), but not in rostral areas of the hypothalamus. Quantitative analysis of GnRH and kisspeptin fibres in the ME revealed a higher innervation density of kisspeptin than of GnRH fibres. The physiological significance of the anatomical findings reported here for the ovulatory mechanism in llamas is still to be determined.

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Silva, L., H. Sánchez, W. Acosta, E. Portiansky, and G. Zuccolilli. "GnRH NEURONES POPULATION IN THE DIENCEPHALON OF THE COYPU (Myocastor coypus)." Revista chilena de anatomía 18, no. 1 (2000). http://dx.doi.org/10.4067/s0716-98682000000100001.

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Suetomi, Yuta, Ryoki Tatebayashi, Shuhei Sonoda, et al. "Establishment of immortalised cell lines derived from female Shiba goat KNDy and GnRH neurones." Journal of Neuroendocrinology 32, no. 6 (2020). http://dx.doi.org/10.1111/jne.12857.

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Ivanova, Deyana, Xiao Feng Li, Caitlin McIntyre, and Kevin Thomas O’Byrne. "SUN-LB49 Chronic Exposure to Predator Odour Stress Disrupts LH Pulsatility and Delays Puberty While Activation of Amygdala Kisspeptin Advances Puberty." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.2143.

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Abstract Chronic exposure to predator odour stress disrupts LH pulsatility and delays puberty whileactivation of amygdala kisspeptin advances pubertyDeyana Ivanova MS1, Xiao Feng Li MD/PhD1, Caitlin Mcintyre BS1, and Kevin O’Byrne PhD1; 1Department of Women and Children’s Health, Faculty of Life Science and Medicine, King’sCollege London, UKPost-traumatic stress (PTSD) is associated with altered pubertal timing and predator odourexposure is a classical rodent PTSD model. Kisspeptin neurones in the posterodorsal sub-nucleus of the medial amygdala (MePD) are thought to modulate pubertal timing and anxiety.We test the hypothesis that psychosocial stress, processed by the MePD, is relayed to theGnRH pulse generator to delay puberty. Female mice were exposed to predator odour, 2,4,5-Trimethylthiazole (TMT), for 14 days from postnatal day (pnd) 21 and pubertal onset wasmonitored. Anxiety was tested using the Elevated Plus Maze (EPM), Light/Dark Box (LDB) andsocial interaction (SI). The effect of TMT on luteinizing hormone (LH) pulses was measured,on pnd 26 and 29. Additionally, kisspeptin-cre mice were bilaterally injected with hM3Dq-DREADD AAV in the MePD at pnd 13. From pnd 21, CNO was administered via drinking waterfor 14 days and pubertal onset was monitored. The TMT-mice showed a significant delay offirst estrous (FE; TMT: 38.1 ± 0.5 vs. control: 33.3 ± 0.6 days; p<0.0001; n=10-14) withoutaffecting body weight (BW; p=0.9; n=10-14). TMT-mice spent less time exploring the openarm of the EPM (TMT: 13 ± 3 vs. control: 32 ± 5 secs; p<0.05; n=10-14) and in the lightcompartment of the LDB (TMT: 117 ± 12 vs. control: 162 ± 15 secs; p<0.05; n=10-14), whileengaging less in SI (TMT: 26.8 ± 2.8 vs. control: 47.7 ± 8.8 secs; p<0.05; n=10-14) during TMT-exposure compared to controls. The TMT group exhibited a reduction in LH pulse frequencyon pnd 26 (TMT: 0.2 ± 0.2 vs. control: 1.7 ± 0.4 pulses/2 h; p<0.05; n=6-9) and 29 (TMT: 0.6 ±0.2 vs. control: 2.6 ± 0.4 pulses/2 h; p<0.001; n=6-9). DREADD activation of kisspeptinneurones in the MePD advances FE (DREADD: 30 ± 1 vs. control 34.67 ± 0.82 days; p<0.05;n=6) without affecting BW (p=0.9; n=6). Predator odour stress reduces GnRH pulse generatorfrequency, delays puberty and enhances anxiety-like behaviour, while selective chemogeneticactivation of kisspeptin neurones in the MePD advances puberty in female mice.

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