Stress and Memory
Stress acutely causes increased delivery of Glucose to the brain, making more energy available to neurons, and therefore better memory formation and retrieval. (Location 3513)
Moderately elevated Glucocorticoids levels facilitate long-term potentiation. Your taste buds, your olfactory receptors, the cochlear cells in your ears all require less stimulation to get excited under moderate stress. (Location 3517)
==The retrieval of prior memories seems more vulnerable to stress than the formation of new ones.== (Location 3538)
A few days of high doses of synthetic glucocorticoids impairs explicit memory in healthy volunteers. (Location 3549)
High glucocorticoid levels enhance something called long-term depression, which might be a mechanism underlying the process of forgetting, the flip side of hippocampal aha-ing. (Location 3566)
The Hippocampus has large amounts of two different types of receptors for Glucocorticoids. Critically, the hormone is about ten times better at binding to one of the receptors (thus termed a “high-affinity” receptor) than the other. Activation of the high-affinity receptor enhances long-term potentiation, while activation of the low-affinity one does the opposite. This is the basis of the inverse-U property: moderate stress helps memory, severe stress harms it. (Location 3570)
⇒ Glucocorticoids
A few weeks of stress or of exposure to excessive glucocorticoids, those cables begin to shrivel, to atrophy and retract a bit. Moreover, the same can occur in the primate brain. When that happens, synaptic connections get pulled apart and the complexity of your neural networks declines. Fortunately, at the end of the stressful period, the neurons can dust themselves off and regrow those connections. (Location 3589)
The Hippocampus is one of only two sites in the brain where new neurons originate. The rate of neurogenesis can be regulated. Learning, an enriched environment, exercise, or exposure to estrogen all increase the rate of neurogenesis, while ==the strongest inhibitors identified to date are, you guessed it, stress and Glucocorticoids.== (Location 3601)
What if the stressor continues? By about thirty minutes into a continuous stressor, glucose delivery is no longer enhanced, and has returned to normal levels. If the stressor goes on even longer, the delivery of glucose to the brain is even inhibited, particularly in the hippocampus—about 25 percent, due to glucocorticoids. (Location 3611)
The higher the glucocorticoid levels at the time of a seizure, the more hippocampal neurons will die. (Location 3617)
The extent of glucocorticoid exposure over the rat’s lifetime not only determined how much hippocampal degeneration there would be in old age, but how much memory loss as well. (Location 3637)
==Soldiers exposed to severe and repeated carnage in combat, individuals repeatedly abused as children—have smaller hippocampi.== (Location 3653)
⇒ PTSD
The shorter the average time allowed to recover from each large bout of jet lag over a career, the smaller the hippocampus and the more memory problems. (Location 3662)
Those whose glucocorticoid levels have been rising over the years since the study began are the ones who have had the most severe loss of hippocampal volume and the greatest decline in memory. (Location 3665)
For the same severity of a stroke, the higher the glucocorticoid levels in a person at the time they come into an emergency room, the more ultimate neurological impairment. (Location 3669)
It suggested instead that having a small hippocampus comes before the PTSD and, in fact, makes you more likely to develop PTSD when exposed to trauma. (Location 3677)
When glucocorticoids cause the cables connecting neurons to shrivel up, it is not a permanent process—stop the glucocorticoid excess and the processes can slowly regrow. The volume losses in PTSD and major depression, however, appear to be something approaching permanent. (Location 3689)
see also
Tags: neuroscience science
Superlink: 050 🧠Neuroscience 051 ☣Neurobiology
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Erstellt: 05-04-26 10:00