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Deyana Ivanova Department of Women and Children’s Health, Faculty of Life Science and Medicine, King’s College London, UK
Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Kevin T O’Byrne Department of Women and Children’s Health, Faculty of Life Science and Medicine, King’s College London, UK

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The exact neural construct underlying the dynamic secretion of gonadotrophin-releasing hormone (GnRH) has only recently been identified despite the detection of multiunit electrical activity volleys associated with pulsatile luteinising hormone (LH) secretion four decades ago. Since the discovery of kisspeptin/neurokinin B/dynorphin neurons in the mammalian hypothalamus, there has been much research into the role of this neuronal network in controlling the oscillatory secretion of gonadotrophin hormones. In this review, we provide an update of the progressive application of cutting-edge techniques combined with mathematical modelling by the neuroendocrine community, which are transforming the functional investigation of the GnRH pulse generator. Understanding the nature and function of the GnRH pulse generator can greatly inform a wide range of clinical studies investigating infertility treatments.

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XiaoFeng Li First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

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Bei Shao First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

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ChengCheng Lin First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

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Kevin T O'Byrne First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

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YuanShao Lin First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
First Department of Neurology, Division of Women's Health, Department of Surgery Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China

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Stress exerts profound inhibitory effects on reproductive function by suppression of the pulsatile release of GnRH and therefore LH. Besides the corticotrophin-releasing factor (CRF), this effect also might be mediated via GABAergic signaling within the arcuate nucleus (ARC) since its inhibitory effects on LH pulses and increased activity during stress. In the present study, we investigated the role of endogenous GABAergic signaling within the ARC in stress-induced suppression of LH pulses. Ovariectomised oestradiol-replaced rats were implanted with bilateral and unilateral cannulae targeting toward the ARC and lateral cerebral ventricle respectively. Blood samples (25 μl) were taken via chronically implanted cardiac catheters every 5 min for 6 h for measurement of LH pulses. Intra-ARC infusion of GABAA receptor antagonist, bicuculline (0.2 pmol in 200 nl artificial cerebrospinal fluid (aCSF) each side, three times at 20-min intervals) markedly attenuated the inhibitory effect of lipopolysaccharide (LPS; 25 μg/kg i.v.) but not restraint (1 h) stress on pulsatile LH secretion. In contrast, restraint but not LPS stress-induced suppression of LH pulse frequency was reversed by intra-ARC administration of GABABR antagonist, CGP-35348 (1.5 nmol in 200 nl aCSF each side, three times at 20-min intervals). Moreover, intra-ARC application of either bicuculline or CGP-35348 attenuated the inhibitory effect of CRF (1 nmol in 4 μl aCSF, i.c.v.) on the LH pulses. These data indicate a pivotal and differential role of endogenous GABAA and GABAB signaling mechanisms in the ARC with respect to mediating immunological and psychological stress-induced suppression of the GnRH pulse generator respectively.

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