Stress Disturbs Cognitive Function

http://www.nature.com/nrn/journal/v3/n6/abs/nrn849_fs.html

THE STRESSED HIPPOCAMPUS, SYNAPTIC PLASTICITY AND LOST MEMORIES
Jeansok J. Kim & David M. Diamond

Abstract

Stress is a biologically significant factor that, by altering brain cell properties, can disturb cognitive processes such as learning and memory, and consequently limit the quality of human life. Extensive rodent and human research has shown that the hippocampus is not only crucially involved in memory formation, but is also highly sensitive to stress. So, the study of stress-induced cognitive and neurobiological sequelae in animal models might provide valuable insight into the mnemonic mechanisms that are vulnerable to stress. Here, we provide an overview of the neurobiology of stress–memory interactions, and present a neural–endocrine model to explain how stress modifies hippocampal functioning.

Summary

• Stress can disturb cognitive processes such as learning and memory, and consequently limit the quality of human life. This review provides an overview of the neurobiology of stress–memory interactions, and presents a neural–endocrine model to explain how stress modifies hippocampal functioning.
• Stress can be defined as a condition in which an individual is aroused by an aversive situation, and its consequences are influenced greatly by the individual's perception of his or her ability to control the presence or intensity of the stimulus.
• The hippocampus is involved in both memory and the neuroendocrine regulation of stress hormones. Hippocampal functions, such as learning and memory, are susceptible to disruption by stress, mediated in part by the activation of type II corticosteroid (glucocorticoid) receptors.
• The primary physiological model of memory is long-term potentiation (LTP), and in vitro and in vivo electrophysiological studies have shown that stress interferes with the induction of hippocampal LTP.
• In addition to affecting synaptic plasticity and memory, stress and corticosterone have been shown to alter hippocampal dendritic morphology and inhibit neurogenesis in the adult brain, which can also have an impact on memory-related functioning.
• The full expression of stress effects on the hippocampus seems to require co-activation of the amygdala and hippocampus, in concert with the direct actions on the hippocampus of neuromodulators, such as corticosterone, 5-hydroxytryptamine, opiates and corticotropin-releasing factor.
• The key assumption of the neuroendocrine model is that alterations in hippocampal functioning after stress are due to an excessive activity exerted by the amygdala on the hippocampus.