![]() Both estrogen and progesterone exert acute effects on synaptic physiology through the activation of multiple intracellular signaling pathways (Minami et al., 1990 Krebs et al., 2000 Wu et al., 2005), including the MAPK/ERK and the Akt pathway which are both part to a non-genomic signaling cascade linked to the promotion of cell survival (Singh, 2001). While these genomic actions of sex hormones require a comparably long time-from minutes to hours-and are limited by the rate of protein biosynthesis, non-genomic modulation of the membrane receptors is mostly faster and requires only milliseconds to seconds (McEwen, 1991 Cornil et al., 2006). Ovarian hormones can act on multiple receptor types, such as voltage-gated ion channels, including GABA A (Gulinello et al., 2001), NMDA (Foy et al., 1999), serotonin (Sumner and Fink, 1998) and dopamine (Becker, 1990) receptors. The classical estrogen receptors (ERα/β) (Gundlah et al., 2001 Mitra et al., 2003) and progesterone receptors (PR A/B) (Brinton et al., 2008) are highly expressed in brain areas involved in emotion and cognition, such as amygdala and hippocampus. Specific structural effects of estrogen and progesterone include neurite outgrowth and synaptogenesis (Haraguchi et al., 2012), dendritic branching (Cooke and Woolley, 2005) and myelination (Garcia-Segura and Melcangi, 2006).īoth estrogen and progesterone act via classical genomic receptors as well as non-classical membrane-associated receptors (see Table S1 for overview on main genomic and non-genomic signaling properties). Furthermore, several lines of evidence support a main impact of sex hormones on brain development and plasticity (Marino et al., 2006). Many of these actions occur in brain regions involved in learning (Hu et al., 2007) and memory (Liu et al., 2008), emotion (Amin et al., 2006), motivation (Sakaki and Mather, 2012), motor control (Horstink et al., 2003), and cognition (Berman et al., 1997). The trophic effects of ovarian hormones emerge early in brain development and remain throughout adolescence (Juraska et al., 2013) and adulthood (Wise et al., 2008). Both hormones provide specific neuroendocrine conditions through which brain structure and function are modulated across a woman's life span. The brain represents an important target for estrogen and progesterone effects. Over the last decades, several lines of research have extended the pivotal actions of ovarian hormones such as estrogen and progesterone outside of the reproductive tract. Finally, we discuss how physiologically occurring hormonal transition periods in humans can be used to model how changes in sex hormones influence functional connectivity, neurotransmission and brain structure in vivo. As the hippocampus is of particular relevance in the context of mediating structural plasticity in the adult brain, we put particular emphasis on what evidence could be gathered thus far that links differences in behavior, neurochemical patterns and hippocampal structure to a changing hormonal environment. Many brain regions have been demonstrated to express high densities for estrogen- and progesterone receptors, such as the amygdala, the hypothalamus, and the hippocampus. We provide an overview of accumulating data during physiological and pathological conditions and discuss currently conceptualized theories on how sex hormones potentially trigger neuroplasticity changes through these four neurochemical systems. Here we review the evidence from animal experiments and human studies reporting interactions between sex hormones and the dominant neurotransmitters, such as serotonin, dopamine, GABA and glutamate. Sex hormones have been implicated in neurite outgrowth, synaptogenesis, dendritic branching, myelination and other important mechanisms of neural plasticity. ![]()
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