Robert M. Sapolsky Quote
Stress and glucocorticoids have inverted-U effects here as well. Moderate, transient stress (or exposure to the equivalent glucocorticoid levels) increases spine number in the hippocampus; sustained stress or glucocor-ticoid exposure does the opposite.7 Moreover, major depression or anxiety—two disorders associated with elevated glucocorticoid levels—can reduce hippocampal dendrite and spine number. This arises from decreased levels of that key growth factor mentioned earlier this chapter, BDNF. Sustained stress and glucocorticoids also cause dendritic retraction and synapse loss, lower levels of NCAM (a neural cell adhesion molecule that stabilizes synapses), and less glutamate release in the frontal cortex.
Robert M. Sapolsky
Stress and glucocorticoids have inverted-U effects here as well. Moderate, transient stress (or exposure to the equivalent glucocorticoid levels) increases spine number in the hippocampus; sustained stress or glucocor-ticoid exposure does the opposite.7 Moreover, major depression or anxiety—two disorders associated with elevated glucocorticoid levels—can reduce hippocampal dendrite and spine number. This arises from decreased levels of that key growth factor mentioned earlier this chapter, BDNF. Sustained stress and glucocorticoids also cause dendritic retraction and synapse loss, lower levels of NCAM (a neural cell adhesion molecule that stabilizes synapses), and less glutamate release in the frontal cortex.
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About Robert M. Sapolsky
Robert Morris Sapolsky (born April 6, 1957) is an American academic and neuroscientist. He is the John A. and Cynthia Fry Gunn Professor at Stanford University, and is a professor of biology, neurology, and neurosurgery. His research has focused on neuroendocrinology, particularly relating to stress. He is also a research associate at the National Museums of Kenya.