The protective effect of estrogen on the central nervous system via the estrogen receptor (ER) has been reported in a number of studies. For example, the use of the ERα ligand, also termed E2, in the treatment of experimental autoimmune encephalomyelitis may reduce the severity of this condition 1).
E2 may also reduce ATP-mediated calcium influx into the primary sensory neurons of mice
Furthermore, E2 may reduce apoptosis in rat astrocytoma cells via the ER
ER, which is a member of the nuclear hormone family of intracellular receptors
G protein coupled estrogen receptor (GPER) (GPR30), which is a member of the rhodopsin-like family of G protein-coupled receptors.
Once activated by estrogen, the ER is able to translocate into the nucleus and bind to DNA to regulate the activity of different genes (i.e. it is a DNA-binding transcription factor). However, it also has additional functions independent of DNA binding.