Our appreciation that estrogens are important neurotrophic and neuroprotect
ive factors has grown rapidly. Although a thorough understanding of the mol
ecular and cellular mechanisms that underlie this effect requires further i
nvestigation, significant progress has been made due to the availability of
animal models in which we can test potential candidates. It appears that e
stradiol can act via mechanisms that require classical intracellular recept
ors (estrogen receptor alpha or beta) that affect transcription, via mechan
isms that include cross-talk between estrogen receptors and second messenge
r pathways, and/or via mechanisms that may involve membrane receptors or ch
annels. This area of research demands attention since estradiol may be an i
mportant therapeutic agent in the maintenance of normal neural function dur
ing aging and after injury. (C) 2001 Academic Press.