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Transcript
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.
