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      Norepinephrine suppresses gonadotropin-releasing hormone (GnRH) neuron excitability in the adult mouse

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      1 , 2 , 2
      Endocrinology

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          Abstract

          Norepinephrine (NE) is considered to exert an important modulatory influence upon the activity of gonadotropin-releasing hormone (GnRH) neurons. In the present study we used a transgenic GnRH-green fluorescent protein mouse model to examine the effects of NE on the electrical excitability of GnRH neurons in male and female mice. Gramicidin-perforated patch recordings demonstrated that NE (10-100µM) exerted a robust membrane hyperpolarization, with associated suppression of firing, in >85% of male prepubertal and adult GnRH neurons (n=25). The same hyperpolarizing action was observed in female GnRH neurons from diestrous (91%, n=11), proestrous (50%, n=14), estrous (77%, n=13) and ovariectomized mice (82%, n=11). A sub-population (<10%) of silent GnRH neurons in all groups responded to NE with hyperpolarization followed by the initiation of firing upon NE washout. The hyperpolarizing actions of NE were mimicked by α1 (phenylephrine) and β (isoproterenol) adrenergic receptor agonists, but α2 receptor activation (guanabenz) had no effect. Approximately 75% of the NE-evoked hyperpolarization was blocked by the α1 receptor antagonist prazosin, and 75% of GnRH neurons responded to both phenylephrine and isoproterenol. These findings indicate that NE acts through both α1 and β adrenergic receptors located on the soma/dendrites of GnRH neurons to directly suppress their excitability throughout the estrous cycle and following ovariectomy. These data force a re-analysis of existing models explaining the effects of NE on gonadotropin secretion.

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          Author and article information

          Journal
          0375040
          3530
          Endocrinology
          Endocrinology
          Endocrinology
          0013-7227
          1945-7170
          14 August 2018
          13 December 2007
          March 2008
          21 August 2018
          : 149
          : 3
          : 1129-1135
          Affiliations
          [1 ]Department of Oral Physiology and Institute of Oral Bioscience, School of Dentistry, Chonbuk National University, Jeonju, South Korea
          [2 ]Centre for Neuroendocrinology and Department of Physiology, University of Otago School of Medical Sciences, Dunedin, New Zealand
          Author notes
          Correspondence to: Allan E. Herbison, Centre for Neuroendocrinology, Department of Physiology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New Zealand, Telephone -64-3-479 7312, Fax -64-3-479 7323, allan.herbison@ 123456otago.ac.nz
          Article
          PMC6103434 PMC6103434 6103434 ems79015
          10.1210/en.2007-1241
          6103434
          18079196
          e25ba2a1-6827-42d2-9d2d-89b0b94810fe
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