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Navarro, Victor

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Navarro

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Victor

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Navarro, Victor

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2012 - 20184

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Author's Publications: search.filters.isAuthorOfPublication.60f045eb-5ad6-418c-9ddb-a73a85e73e02

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Now showing 1 - 4 of 4
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    PACAP neurons in the ventral premammillary nucleus regulate reproductive function in the female mouse
    (eLife Sciences Publications, Ltd, 2018) Ross, Rachel; Leon, Silvia; Madara, Joseph; Schafer, Danielle; Fergani, Chrysanthi; Maguire, Caroline A; Verstegen, Anne; Brengle, Emily; Kong, Dong; Herbison, Allan E; Kaiser, Ursula; Lowell, Bradford; Navarro, Victor
    Pituitary adenylate cyclase activating polypeptide (PACAP, Adcyap1) is a neuromodulator implicated in anxiety, metabolism and reproductive behavior. PACAP global knockout mice have decreased fertility and PACAP modulates LH release. However, its source and role at the hypothalamic level remain unknown. We demonstrate that PACAP-expressing neurons of the ventral premamillary nucleus of the hypothalamus (PMVPACAP) project to, and make direct contact with, kisspeptin neurons in the arcuate and AVPV/PeN nuclei and a subset of these neurons respond to PACAP exposure. Targeted deletion of PACAP from the PMV through stereotaxic virally mediated cre- injection or genetic cross to LepR-i-cre mice with Adcyap1fl/fl mice led to delayed puberty onset and impaired reproductive function in female, but not male, mice. We propose a new role for PACAP-expressing neurons in the PMV in the relay of nutritional state information to regulate GnRH release by modulating the activity of kisspeptin neurons, thereby regulating reproduction in female mice.
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    Effects of intravenous administration of neurokinin receptor subtype-selective agonists on gonadotropin-releasing hormone pulse generator activity and luteinizing hormone secretion in goats
    (The Society for Reproduction and Development, 2015) YAMAMURA, Takashi; WAKABAYASHI, Yoshihiro; OHKURA, Satoshi; Navarro, Victor; OKAMURA, Hiroaki
    Recent evidence suggests that neurokinin B (NKB), a member of the neurokinin (tachykinin) peptide family, plays a pivotal role in gonadotropin-releasing hormone (GnRH) pulse generation. Three types of neurokinin receptors (NKRs), NK1R, NK2R and NK3R, are found in the brain. Although NKB preferentially binds to NK3R, other NKRs are possibly also involved in NKB action. The present study examined the effects of intravenous administration of the NKR subtype-selective agonists GR73632 (NK1R), GR64349 (NK2R), and senktide (NK3R) on GnRH pulse generator activity and luteinizing hormone (LH) secretion. Multiple-unit activity (MUA) was monitored in ovariectomized goats (n = 5) implanted with recording electrodes. Characteristic increases in MUA (MUA volleys) were considered GnRH pulse generator activity. Although three NKR agonists dose-dependently induced an MUA volley and an accompanying increase in LH secretion, the efficacy in inducing the volley markedly differed. As little as 10 nmol of senktide induced an MUA volley in all goats, whereas a dose of 1000 nmol was only effective for the NK1R and NK2R agonists in two and four goats, respectively. When the treatment failed to evoke an MUA volley, no apparent change was observed in the MUA or LH secretion. Similar effects of the NK2R and NK3R agonists were observed in the presence of estradiol. The results demonstrated that NK3R plays a predominant role in GnRH pulse generation and suggested that the contributions of NK1R and NK2R to this mechanism may be few, if any, in goats.
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    New Insights into the Control of Pulsatile GnRH Release: The Role of Kiss1/Neurokinin B Neurons
    (Frontiers Research Foundation, 2012) Navarro, Victor
    Gonadotropin-releasing hormone (GnRH) is the ultimate output signal of an intricate network of neuroendocrine factors that, acting on the pituitary, trigger gonadotropin release. In turn, gonadotropins exert their trophic action on the gonads to stimulate the synthesis of sex steroids thus completing the gonadotropic axis through feedback regulatory mechanisms of GnRH release. These feedback loops are predominantly inhibitory in both sexes, leading to tonic pulsatile release of GnRH from puberty onward. However, in the female, rising levels of estradiol along the estrous cycle evoke an additional positive feedback that prompts a surge-like pattern of GnRH release prior to ovulation. Kisspeptins, secreted from hypothalamic Kiss1 neurons, are poised as major conduits to regulate this dual secretory pathway. Kiss1 neurons are diverse in origin, nature, and function, convening distinct neuronal populations in two main hypothalamic nuclei: the arcuate nucleus (ARC) and the anteroventral periventricular nucleus. Recent studies from our group and others point out Kiss1 neurons in the ARC as the plausible generator of GnRH pulses through a system of pulsatile kisspeptin release shaped by the coordinated action of neurokinin B (NKB) and dynorphin A (Dyn) that are co-expressed in Kiss1 neurons (so-called KNDy neurons). In this review, we aim to document the recent findings and working models directed toward the identification of the Kiss1-dependent mechanisms of GnRH release through a synoptic overview of the state-of-the-art in the field.
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    Altered Circadian Feeding Behavior and Improvement of Metabolic Syndrome in Obese Tac1-Deficient Mice
    (Springer Science and Business Media LLC, 2017-12) Maguire, Caroline; Leon, Silvia; Carroll, Rona; Kaiser, Ursula; Navarro, Victor
    BACKGROUND Metabolic function is regulated by the interplay of central and peripheral factors that ultimately regulate food intake and energy expenditure. The tachykinin substance P (SP) has been identified as a novel regulator of energy balance, however, the mechanisms underlying this effect are ill-defined and conflicting data regarding the role of SP on food intake have been reported by different groups. OBJECTIVE To further characterize the metabolic role of the Tac1 gene products (SP and neurokinin A (NKA)) in mice through a series of genetic, metabolic and behavioral studies in Tac1 deficient mice. RESULTS Tac1−/− mice are leaner than controls and display reduced food intake and altered feeding circadian rhythm, supported by disrupted expression of the clock genes Cry1/2, Per1/2 in the suprachiasmatic nucleus (SCN), medio-basal hypothalamus (MBH) and liver, as well as increased Pomc expression in the MBH. Tac1 ablation induced resistance to obesity, improved glucose tolerance, prevented insulin resistance under high-fat-diet, increased activation of brown adipose tissue and improved hepatic steatosis. Moreover, deletion of Tac1 in ob/ob mice ameliorated BW gain in females only but was sufficient to decrease fat and triglyceride content in the liver of males. CONCLUSIONS These results provide further evidence that Tac1 controls circadian feeding behavior and metabolism in mice through mechanisms that involve the regulation of the melanocortin system. In addition, these studies suggest that the blockade of SP may offer a new method to treat metabolic syndrome.