17β-oestradiol regulation of gonadotrophin-releasing hormone neuronal Excitability

O. K. Rønnekleiv, M. A. Bosch, C. Zhang

Research output: Contribution to journalReview article

16 Scopus citations

Abstract

17β-Oestradiol (E 2) is essential for cyclical gonadotrophin-releasing hormone (GnRH) neuronal activity and secretion. In particular, E 2 increases the excitability of GnRH neurones during the afternoon of pro-oestrus in the rodent, which is associated with increased synthesis and secretion of GnRH. It is well established that E 2 regulates the activity of GnRH neurones through both presynaptic and postsynaptic mechanisms. E 2 significantly modulates the mRNA expression of numerous ion channels in GnRH neurones and alters the associated endogenous conductances, including potassium (K ATP, A-type) currents and low-voltage T-type and high-voltage L-type calcium currents. Notably, K ATP channels are critical for maintaining GnRH neurones in a hyperpolarised state for recruiting the T-type calcium channels, which are important for burst firing in GnRH neurones. In addition, there are other critical channels contributing to burst firing pattern, including the small conductance Ca 2+-activated K + channels that may be modulated by E 2. Despite these advances, the cellular mechanisms underlying the cyclical GnRH neuronal activity and GnRH release are largely unknown. Ultimately, the ensemble of both pre- and postsynaptic targets of the actions of E 2 will dictate the excitability and activity pattern of GnRH neurones.

Original languageEnglish (US)
Pages (from-to)122-130
Number of pages9
JournalJournal of Neuroendocrinology
Volume24
Issue number1
DOIs
StatePublished - Jan 1 2012

Keywords

  • Burst firing
  • Gonadotrophin-releasing hormone neurones
  • Hyperpolarisation
  • T-type calcium channels

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

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