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Brain-derived estrogen and neural function
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<blockquote data-quote="madman" data-source="post: 212632" data-attributes="member: 13851"><p><strong>Fig. 5. <u>Schematic illustration of the potential mechanisms underlying neuron-derived E2 (NDE2) regulation of synaptic plasticity</u>. It is proposed that neuron-derived E2 (NDE2) regulates synaptic plasticity via both rapid and genomic signaling mechanisms. 1) Membrane localized estrogen receptors (estrogen receptorα and β, ERα and ERβ, and G-protein coupled estrogen receptor-1, GPER1) can bind NDE2 and 2) the receptor-bound NDE2 then induces rapid PI3K/AKT and MEK/ERK kinase signaling, which is capable of quickly shaping synaptic plasticity. In addition, the activated intracellular kinase signaling also phosphorylates the important transcriptional factor, CREB which further translocates into the nucleus to facilitate the expressions of neurotrophic factor BDNF and synaptic protein PSD95. BDNF can also regulate synaptic plasticity by coupling to the rapid intracellular kinases. Moreover, BDNF signaling activates cofilin which is required for F-actin assembly and dendritic spine formation. Intracellular ERα and ERβ act in the genomic signaling pathway by transactivating estrogen response elements (ERE) in regulated genes and promoting genes transcription. CRE = cAMP response element.</strong></p><p><strong>[ATTACH=full]17921[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 212632, member: 13851"] [B]Fig. 5. [U]Schematic illustration of the potential mechanisms underlying neuron-derived E2 (NDE2) regulation of synaptic plasticity[/U]. It is proposed that neuron-derived E2 (NDE2) regulates synaptic plasticity via both rapid and genomic signaling mechanisms. 1) Membrane localized estrogen receptors (estrogen receptorα and β, ERα and ERβ, and G-protein coupled estrogen receptor-1, GPER1) can bind NDE2 and 2) the receptor-bound NDE2 then induces rapid PI3K/AKT and MEK/ERK kinase signaling, which is capable of quickly shaping synaptic plasticity. In addition, the activated intracellular kinase signaling also phosphorylates the important transcriptional factor, CREB which further translocates into the nucleus to facilitate the expressions of neurotrophic factor BDNF and synaptic protein PSD95. BDNF can also regulate synaptic plasticity by coupling to the rapid intracellular kinases. Moreover, BDNF signaling activates cofilin which is required for F-actin assembly and dendritic spine formation. Intracellular ERα and ERβ act in the genomic signaling pathway by transactivating estrogen response elements (ERE) in regulated genes and promoting genes transcription. CRE = cAMP response element. [ATTACH type="full"]17921[/ATTACH][/B] [/QUOTE]
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Brain-derived estrogen and neural function
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