Hormones Controls of V-SVZ Neurogenesis into the Mature Female

In conclusion, many circumstances make a difference to adult neurogenesis from the V-SVZ-OB system, and is also possible that a number of them try sexually dimorphic and alter throughout existence

Typically, estrogens are neuroprotective and trigger differentiation and expansion when you are progestins and you will androgens turn on differentiation and phone success (21). Yet not, the V-SVZ-OB system has its unique keeps. In this visualize, the latest urinary system may gamble an option character.

Circulating hormone levels dramatically change during the life of female rodents, during both estrous cycle and pregnancy. These changes may affect neurogenesis. In particular, E₂ levels control the estrous cycle, pregnancy, and sexual behavior (32, 55).

Since OB has a key role in mother’s offspring recognition, it is not surprising that the rate of neurogenesis in V-SVZ transiently increase during pregnancy (56). Indeed, two peaks of cell proliferations were observed at gestation day 7 and at postpartum day 7, while at delivery the neurogenic rate is similar to matched aged virgin females (56). The first peak is evident also in females mated with sterile males, so it depends on maternal hormonal levels rather than on the embryo. However, this effect is mediated by prolactin rather than E₂ or progesterone (56, 57). However, E₂ may have an indirect role, since it stimulates prolactin release (58).

In the adult female mouse, E₂ has an inhibitory effect on V-SVZ-OB neurogenesis in both V-SVZ and OB. First, it decreases cell proliferation in the V-SVZ in different models. The number of proliferating cells in the V-SVZ is lower during estrus, than proestrus (39). Moreover, in ovariectomized females, acute E₂ supplementation for one day, with a dose comparable to the estrus, decreases cell proliferation in the V-SVZ (59). On the other hand, this effect was not detected by long-term treatment [3 weeks (60)] or with a lower dose of E₂ (61), comparable with diestrus (62). Differences in the effect of ovariectomy may be due to an interplay of many component of the neural stem-cell niche. ₂ supplementation selectively upregulates ER? (51). T metabolite 5?-dihydrotestosterone (5?DHT) decreases the expression of AR in the choroid plexus of ovariectomized mice (51).

Male pheromones stimulate the production of ovarian hormones (63) as well as the neurogenesis in adult females (35, 64, 65). However, E₂ does not increase neurogenesis (66), nor cell proliferation in V-SVZ or neuroblasts density in OB, but it decreases cell survival in AOB, but not in MOB (24).

In the OB, E₂ has different effects depending on the region. In the MOB, in adulthood rather than during development, E₂ is able to impair the survival of newly generated cells (59) and MOB functionality (60) . Interestingly, as demonstrated in aromatase-KO mice, developmental E₂ has the opposite effect in the AOB: the absence of E₂ during development decreases the survival of adult generated cells in the AOB. This phenotype can be reverted by adult E₂ treatment. On the contrary, the lack of estrogens during development neither alters cell proliferation in the V-SVZ, nor its response to E₂ (60).

Actually, ovariectomized mice share one another ER? and you may ER?, however, E

In contrast to mice, the proliferation rate in the rat V-SVZ does not change during pregnancy, while it increases at delivery (67). As for mice, E₂ role in female rat is highly debated. Proliferation in the V-SVZ is not affected neither by ovariectomy nor by acute T or E₂ supplementation (41). No studies are available on the long-term effects of ovariectomy despite it deeply alter choroid plexus transcriptome which may indirectly affect the neural stem-cell niche (68). However, E₂ decreases the survival of newly generated cells in the AOB, but not in the MOB [(29, 30); Figure 2; Table 2].