The hippocampus is a target of stress hormones, and it is an especially pla
stic and vulnerable region of the brain. It also responds to gonadal, thyro
id, and adrenal hormones, which modulate changes in synapse formation and d
endritic structure and regulate dentate gyrus volume during development and
in adult life. Two forms of structural plasticity are affected by stress:
Repeated stress causes atrophy of dendrites in the CA3 region, and both acu
te and chronic stress suppresses neurogenesis of dentate gyrus granule neur
ons. Besides glucocorticoids, excitatory amino acids and N-methyl-D-asparta
te (NMDA) receptors are involved in these two forms of plasticity as well a
s in neuronal death that is caused in pyramidal neurons by seizures and by
ischemia. The two forms of hippocampal structural plasticity are relevant t
o the human hippocampus, which undergoes a selective atrophy in a number of
disorders, accompanied by deficits in declarative, episodic, spatial, and
contextual memory performance. It is important, from a therapeutic standpoi
nt, to distinguish between a permanent loss of cells and a reversible atrop
hy.