Download HPA Axis Activation and Hippocampal Atrophy

HPA Axis Activation and Hippocampal Atrophy
Author :
Albert Maramis
Abstract :
HPA axis activation begins with an increase in Corticotropin-Releasing Hormone (CRH) secretion
by Paraventricular Nucleus (PVN) in hypothalamus and results in the release of adrenal cortex
hormone, cortisol. Higher centers, such as cortex and limbic system, also involve in this
reaction, especially the amygdala and hippocampus. Generally, hippocampus has inhibiting
effect towards HPA axis. On the other hand, central nucleus of amygdala involves in the
stimulation of HPA activity by stressors through direct projection to PVN. The lessening of
hippocampal pyramidal neurons was first noticed in aging rats. Adrenalectomy performed on
middle-aged rat can halt this process, while administration of glucocorticoid for 12 weeks
resulted in neuronal loss in hippocampal formation. Chronic social stress can also decrease the
amount of hippocampal neurons in monkeys. This effect differs for various areas in
hippocampus according to the type of stressor. The decrease in hippocampal volume related to
glucocorticoid and stress can be the result of neuronal loss or other structural changes that
does not necessarily mean damage. Recent evidence shows there is reversible function and
structural plasticity in adult hippocampus as the result of adrenal steroid activity. Stressinduced hippocampal atrophy can be blocked by various means: (1) inhibition of release and
action of excitatory amino acids by phenytoin; (2) enhancement of serotonin reuptake by
tianeptine; and (3) inhibition of adrenal steroid synthesis in stress response.