Skip to main content
. Author manuscript; available in PMC: 2010 Oct 1.
Published in final edited form as: Trends Endocrinol Metab. 2009 Sep 7;20(8):402–408. doi: 10.1016/j.tem.2009.05.002

Figure 4.

Figure 4

Expression of ERs in hypothalamic GnRH neurons. Estrogen receptor alpha (ERα) and beta (ERβ) are expressed in cultured hypothalamic GnRH neurons. (i) In cultured hypothalamic cells and immortalized GT1–7 neurons, low (picomolar) E2 concentrations and an ERα agonist suppressed spontaneous action potential (AP) firing, decreased cAMP production, and inhibited pulsatile GnRH release. The marked inhibitory effects of Gi-coupled ERα on spontaneous AP firing, cAMP production, and pulsatile GnRH secretion, indicate its capacity for negative regulation of GnRH neuronal function. (ii) In contrast, higher (nanomolar) E2 concentrations and an ERβ agonist increased the rate of AP firing, cAMP production, and GnRH secretion, consistent with positive regulation of GnRH secretion. In accord with the coupling of ER to PTX-sensitive Gi/o proteins, E2 also activates G protein-activated inwardly rectifying potassium (GIRK) channels, decreasing membrane excitability and slowing the firing of spontaneous APs in hypothalamic GnRH neurons. Green and red lines indicate stimulatory and inhibitory actions, respectively.