Journal
JOURNAL OF NEUROENDOCRINOLOGY
Volume 25, Issue 11, Pages 1219-1230Publisher
WILEY
DOI: 10.1111/jne.12071
Keywords
dendritic spines; neuroprotection; signal transduction; oestrogen receptors; GPER1; 17-oestradiol; oestradiol
Categories
Funding
- Royal Society UK
- National Alliance for Research on Schizophrenia and Depression (NARSAD)
- Psychiatry Research Trust
- BBSRC via the Babraham Institute
- BBSRC [BB/E00153X/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E00153X/1] Funding Source: researchfish
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Oestrogens are now recognised to be able to initiate rapid, fast responses, in addition to their classical, longer-term actions. There is a growing appreciation of the potential implications of this mode of action for oestrogenic signalling in both neuronal and non-neuronal systems. As such, much effort has been made to determine the mechanisms that are critical for transducing these rapid effects into cellular responses. Recently, an orphan G-protein-coupled receptor (GPCR), termed GPR30, was identified as an oestrogen-sensitive receptor in cancer cells. This receptor, now term G-protein oestrogen receptor 1 (GPER1) has been the subject of many investigations, and a role for this receptor in the nervous system is now emerging. In this review, we highlight some of the more recent advances in our understanding of the distribution and subcellular localisation of this receptor in the brain, as well as some of the evidence for the potential role that this receptor may play in the brain. We then discuss some of the controversies surrounding the pharmacology of this receptor, and attempt to reconcile these by suggesting that the agonist-specific coupling' model of GPCR function may provide a potential explanation for some of the divergent reports of GPER1 pharmacology.
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