About You

Estradiol treatment had no effect on cell proliferation in the SVZ of female mice , suggesting that it is not the cause of the sex difference in cell proliferation. Compared to the dentate gyrus, relatively little work has been done testing the effects of testosterone upon neurogenesis in the mammalian olfactory bulbs (Table 1) . Female cowbirds show greater hippocampal neurogenesis than males, and neurogenesis levels peaked after the breeding season was over . Additional experiments with canaries demonstrated that testosterone-induced neurogenesis within the HVC of female canaries was proceeded by enhanced capillary vasculature (angiogenesis) and the production of growth factors 68,69. The high vocal center (HVC) is a component of the song system used for the production and learning of song, and in the adult brain new neurons migrate into this region from the walls of the lateral ventricles in a manner comparable to adult neurogenesis within the olfactory bulbs of rodents .
Additionally, a number of studies have shown that performance on a variety of spatial memory tasks results in increased adult neurogenesis. It is therefore unlikely that the effects of testosterone upon neurogenesis in male rodents involve an estrogen-dependent pathway. Thus, there is some evidence that acute doses of estradiol increase cell proliferation and possibly early neuronal development, but these effects do not correspond with the timing of the neurogenesis-enhancing effects of prolonged testosterone exposure.
Testosterone also appears to relate to brain structural development, but the VBM studies that we reviewed here show modulatory effects by gender, age, and other circulating hormones, and so more research is needed to clarify this area. The association with this brain region appears to be modulated by gender and stage of development (e.g. fetal testosterone exposure, hormone levels during adolescence and adulthood), and future research needs to explore these factors further. When the endogenous testosterone studies were split by sex, the significant activation of the brain stem was seen in the female samples only. Furthermore, we conducted a review of structural MRI i.e. voxel based morphometry (VBM) studies which considered brain volume in relation to testosterone levels in adults and in children. This enhanced survival involves an androgen-dependent pathway in males, distinct from the estrogen-dependent pathway that can increase or decrease neurogenesis in females. Most work to date has been conducted using rats and mice to test the effects of a wide range of testosterone manipulations upon adult neurogenesis in the dentate gyrus. The ability of testosterone to protect against a stress-induced decrease neurogenesis seems to involve sustaining basal cell survival levels and possibly basal cell proliferation levels as well .
In the pathology of PMDD, the normal functioning of predominantly two main neurotransmitter system, the serotonergic and dopaminergic system seems to be impaired. A subgroup of women, however, suffers from clinical level of premenstrual mood changes called premenstrual dysphoric disorder (PMDD), a condition that has recently been included in the DSM-V (Epperson et al., 2012a). The alternation of both mechanisms largely affect the neurochemical systems involved in healthy emotional and cognitive control, such as dopaminergic, serotonergic, glutamatergic and γ-aminobutyric acid (GABA)-ergic systems.
Androgen receptors and androgen receptor mRNAs have been localized within the CA1 sub-region of the hippocampus of adult male rats 169,170. Because steroids are hydrophobic, androgens pass directly through cell membranes to bind to cytoplasmic androgen receptors that dimerize and act as a transcription factors , and the resulting changes in gene transcription could explain the effects of androgens on neurogenesis. Thus, current evidence points to an apparent sex different in the role of sex steroids in regulating hippocampal neurogenesis, with an androgen-dependent pathway playing a dominant regulatory role in males and an estrogen-dependent pathway playing a dominant role in females. The authors speculate that excessive androgen receptors in newly developing neurons may reduce neuronal survival in some way, comparable to some neurogenesis-impairing effects that have been observed with high doses of testosterone 101,102. Similarly, flutamide was shown to block an exercise-induced increase in hippocampal neurogenesis (2-week-old neurons) among male rats, whereas an estrogen-receptor antagonist (tamoxifen) did not .
Like serotonin, dopamine (DA) is a neurotransmitter implicated in reward processing and mood regulation (Diehl and Gershon, 1992; Belujon and Grace, 2017). Using rat derived serotonergic neuronal cell line that expresses SERT and ERβ but lacks ERα, it was shown that E2 application resulted in a reduction of SERT activity (Koldzic-Zivanovic et al., 2004). Likewise, in the rodent dorsal raphe nucleus, tph1 levels were heightened by E2, an effect mediated by ERβ (Gundlah et al., 2005; Nomura et al., 2005).

Profile Info