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. Author manuscript; available in PMC: 2015 Feb 4.
Published in final edited form as: Neuroscientist. 2014 Feb 7;20(5):534–545. doi: 10.1177/1073858413519865

Figure 2.

Figure 2

Simplified models depicting rapid estrogen receptor signaling (left) and classical nuclear pathway (right). (A) In the rapid estrogen receptor signaling pathway, estrogen activates membrane associated estrogen receptors and associated G-protein coupled receptors to induce intracellular signaling cascades, which rapidly influence neuronal physiology or lead to the phosphorylation of the estrogen receptor-alpha (ERα) or CREB proteins. (B) In the classical pathway, estrogen binds to an inactive ERα or ERβ within the cytoplasm or the nucleus of the cell. The activated estrogen receptor monomer forms a dimer with another activated estrogen receptor monomer to create either a homodimer or a heterodimer, which then binds to an estrogen response element (ERE) within the DNA, along with other co-regulator proteins (not shown) to modify transcription of target genes. Note that ERα homodimers exhibit increased transcription relative to estrogen receptor heterodimers or ERβ homodimers because of ERβ acting as a negative regulator of ERα-mediated transcription.