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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Front Neuroendocrinol. 2015 Jan 9;37:43–51. doi: 10.1016/j.yfrne.2014.12.002

Figure 3.

Figure 3

Schematic depiction of the neural circuitry in the hypothalamus regulating seasonal control of estradiol (E2) negative feedback. E2 acts upon ER-alpha containing cells (blue) in the ventromedial preoptic area (POA) and retrochiasmatic area (RCh); these neurons, in turn, stimulate A15 dopamine cells (red) via glutamatergic inputs. A15 dopamine cells project caudally to the mediobasal hypothalamus (MBH) and inhibit GnRH cells (brown) either directly at the level of their terminals in the median eminence, and/or indirectly via kisspeptin (Kiss) cells (green) in the arcuate nucleus. Seasonal plasticity has been demonstrated at several sites in this circuitry including that of glutamatergic contacts onto A15 neurons (42); the dendritic morphology of dopaminergic A15 neurons (43); and the number of kisspeptin inputs to GnRH neurons in the MBH (48). Such morphological changes may result in a functional “reconnection” of this circuitry during anestrus, and underlie the ability of E2 to inhibit GnRH pulse frequency at this time of year. OCh = optic chiasm. (Modified from ref. 27).