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. Author manuscript; available in PMC: 2017 Sep 7.
Published in final edited form as: Neuroscience. 2016 Jun 15;331:62–71. doi: 10.1016/j.neuroscience.2016.06.014

Figure 6. Model for Hindbrain ERβ Regulation of the LH Surge during Insulin-Induced Hypoglycemia.

Figure 6

Estrogen- and metabolic-sensitive hindbrain A2 neurons [Insert C] exhibit singular reactivity to hypoglycemia among medullary catecholamine cell groups, and exhibit elevated ERβ protein during this metabolic stress [Ibrahim and Briski, 2015]. Current data show that hypoglycemic augmentation of A2 DβH protein expression and concurrent suppression of the LH surge are each reversed by intra-CV4 administration of the ERβ antagonist PHTPP. GnRH-I content of the rPO, where perikarya of glucoprivic-responsive GnRH neurons reside [Insert A] was diminished by hypoglycemia, but was not normalized in PHTPP- plus insulin-treated rats. Augmenting effects of hypoglycemia on rPO, AVPV, MPN, and ARH NE levels were reversed only in the latter site by PHTPP, where prepro-kisspeptin content was also normalized by that pretreatment [Insert B]. These results suggest that ERβ-dependent mechanisms may repress the LH surge through mechanisms that target axon terminal neurotransmitter storage, metabolism, and/or release.