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17β‐Oestradiol Regulation of Gonadotrophin‐Releasing Hormone Neuronal Excitability
Author(s) -
Rønnekleiv O. K.,
Bosch M. A.,
Zhang C.
Publication year - 2012
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2011.02160.x
Subject(s) - postsynaptic potential , endocrinology , medicine , gonadotropin releasing hormone , potassium channel , inhibitory postsynaptic potential , endogeny , chemistry , voltage dependent calcium channel , biology , neuroscience , sk channel , hormone , calcium , ion channel , receptor , luteinizing hormone
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.