It has become customary to distinguish between so-called ''genomic'' a
ctions of steroid hormones involving intracellular receptors and ''non
-genomic'' effects of steroids that involve putative cell surface rece
ptors. Whereas there is no doubt that this distinction has considerabl
e validity, it does not go far enough in addressing the variety of mec
hanisms that steroid hormones use to produce their effects on cells. T
his is because cell surface receptors may signal changes in gene expre
ssion, while genomic actions sometimes affect neuronal excitability, o
ften doing so quite rapidly. Moreover, steroid hormones and neurotrans
mitters may operate together to produce effects, and sometimes these e
ffects involve collaborations between groups of neurons. As illustrati
ons, evidence is reviewed in this article that a number of steroid act
ions in the hippocampus involves the co-participation of excitatory am
ino acids. These interactions are evident for the regulation of synapt
ogenesis by estradiol in the CA1 pyramidal neurons of hippocampus and
for the induction of dendritic atrophy of CA3 neurons by repeated stre
ss as well as by glucocorticoid injections. In addition, neurogenesis
in the adult and developing dentate gyrus is ''contained'' by adrenal
steroids as well as by excitatory amino acids. In each of these three
examples, NMDA receptors are involved. These results not only point to
a high degree of interdependency between certain neurotransmitters an
d the actions of steroid hormones but also emphasize the degree to whi
ch structural plasticity is an important aspect of steroid hormone act
ion in the adult as well as developing nervous system. (C) 1994 Academ
ic Press, Inc.