کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4326380 1614075 2010 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Regulation of endogenous conductances in GnRH neurons by estrogens
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Regulation of endogenous conductances in GnRH neurons by estrogens
چکیده انگلیسی
17β-estradiol (E2) regulates the activity of the gonadotropin-releasing hormone (GnRH) neurons through both presynaptic and postsynaptic mechanisms, and this ovarian steroid hormone is essential for cyclical GnRH neuronal activity and secretion. E2 has significant actions to modulate the mRNA expression of numerous ion channels in GnRH neurons and/or to enhance (suppress) endogenous conductances (currents) including potassium (KATP, A-type) and calcium low voltage T-type and high voltage L-type currents. Also, it is well documented that E2 can alter the excitability of GnRH neurons via direct action, but the intracellular signaling cascades mediating these actions are not well understood. As an example, KATP channels are critical ion channels needed for maintaining GnRH neurons in a hyperpolarized state for recruiting T-type calcium channels that are important for burst firing in GnRH neurons. E2 modulates the activity of KATP channels via a membrane-initiated signaling pathway in GnRH neurons. Obviously there are other channels, including the small conductance activated K+ (SK) channels, that maybe modulated by this signaling pathway, but the ensemble of mER-, ERα-, and ERβ-mediated effects both pre- and post-synaptic will ultimately dictate the excitability of GnRH neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1364, 10 December 2010, Pages 25-34
نویسندگان
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