Nsity of thorns. The effect on the improvement estrogen receptor signaling pathway is not spinogenesis gr It at h Higher concentrations of BPA than those with low BPA. BPA Haupts Chlich obtained Ht the density of spines by about Middle Head. 1.5 times. The reason is unclear, selective for the Erh Increase, since the BPA would affect all the thorns. We can not k Exclusively S that BPA small head spines and thorns can head to the middle magnifying your hen Ren erh. Although the receptors are different, a certain amount is Observed similarity between BPA and E2 on the modulation effects on cut spinogenesis adults. The increase in the Middle Head spines also occurs with 1 nM E2 treatment for 2 h in CA1 of the hippocampus. The E2-induced spinogenesis also registered Born of Erk MAP kinase pathway. NMDA receptor blockade by MK-801 abolished the effect of E2 and BPA, suggesting that both E2 and BPA signaling a basic level of Ca 2, which is held by the Ca 2 + influx require with spines via NMDA receptors, since the spontaneous doping. As another example, in organotypic cultures of hippocampal slices, pre-treatment for 24 h with E2 or BPA verst to 10 nM Strengths Notch Pathway CA3 neuronal Sch The caused by glutamate, because spinogenesis verst RKT by E2 or BPA. 4.2. ERRC is a receptor with high affinity t for BPA Although ERA should be a receiver Be singer of BPA in previous studies, the binding affinity t of BPA ERA for much less than that of E2. Therefore, the nanomolar BPA can probably not induce a significant effect on spinogenesis from four centuries. In addition, BPA binds tightly to the ERRC. To identify the receptor induces spinogenesis responsible for the modulation of the EPS, we have OH-Tam, an antagonist of the ERRC / ERA Erb /, and ICI, an antagonist of the ERA / ERB. OH Tam completely Lifted ndig improving spinogenesis of BPA, however, ICI has not improved by the EPS induced spinogenesis removed. This closing S we find that the ERRC is a functional receptor with high affinity t for BPA. Note that bind E2 is not the ERRC. BPA rapidly activated the transcription factor, cAMP response element binding protein in the pancreatic B-cells. Phosphorylated CREB increased rapidly after application of 1 nM BPA Ht. The increase in CREB phosphorylation is not by ICI, which means that ERA / ERB implies not involved in these processes. Until this study, the ERRC not been established as a functional receptor BPA, although the ERRC is presented as a binding site close to BPA. By analyzing the luciferase reporter gene, showing the ERRC constitutive transcriptional activity of t without ligands, including BPA. OH-Tam inhibits the transcriptional activity of t by ERRC ERRC strongly binding with IC50 of 10.9 nM. BPA also has a strong bond with the ERRC with IC50 of 13 nM. BPA antagonizes the activity of t before Tam OH, which then causes no resumption of Transkriptionsaktivit t of the ERRC. In other words, OH Tam, an inverse agonist. BPA is not alone, however, modulate basal high Transkriptionsaktivit t of the ERRC, singer Fostamatinib against the sale of the ERRC BPA as a receiver. Fortunately, in this study we have shown the function of the ERRC as an inducer of spinogenesis in linking BPA. However, it is also m Resembled Ren explained That an endogenous agonist reverse ERRC ERRC inhibited in the absence of BPA, BPA and antagonized the application of the inhibition.