Stress and cognitive function

  title={Stress and cognitive function},
  author={Bruce S. McEwen and Robert Morris Sapolsky},
  journal={Current Opinion in Neurobiology},
Amygdala, Medial Prefrontal Cortex and Glucocorticoid Interactions Produce Stress-Like Effects on Memory
Adverse stress effects on the hippocampal memory system are generally thought to be due to the high level of circulating glucocorticoids directly modifying the properties of hippocampal neurons and,
Neuromodulators of LTP and NCAMs in the amygdala and hippocampus in response to stress.
Possibly, at the onset of an emotional event the stress hormones permissively mediate plasticity and PSA-related synaptic remodeling is mobilized for memory formation in particularly challenging circumstances.
Neural-Cognitive Effects of Stress in the Hippocampus
The effects of stress on three vertically related levels of hippocampal functions-synaptic plasticity, neural activity and memory-and the recent evidence implicating the amygdala as a crucial component of the central stress mechanism are reviewed.
The stressed hippocampus, synaptic plasticity and lost memories
An overview of the neurobiology of stress–memory interactions is provided, and a neural–endocrine model is presented to explain how stress modifies hippocampal functioning.
The Role and Mechanisms of Action of Glucocorticoid Involvement in Memory Storage
  • C. Sandi
  • Biology, Psychology
    Neural plasticity
  • 1998
Certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation.


Glucocorticoid-induced impairment in declarative memory performance in adult humans
Investigation of the cognitive consequences of DEX treatment in normal adult human subjects hypothesizing a decrease in declarative memory performance after extended but not overnight treatment found correct paragraph recall improved over the course of treatment, consistent with practice.
Glucocorticoids, stress and exacerbation of excitotoxic neuron death
Current findings suggest that glucocorticoids impair glucose uptake in the hippocampus, indirectly causing a mild energetic vulnerability in the structure.
Stress, the Aging Brain, and the Mechanisms of Neuron Death
Part 1 The glucocorticoid cascade hypothesis: the stress-response and the emergence of stress-related disease an introduction to the adrenocortical axis glucocorticoid concentrations in the aged rat
β-Adrenergic activation and memory for emotional events
The impairment of propranolol on memory of the emotional story was not due either to reduced emotional responsiveness or to nonspecific sedative or attentional effects, which support the hypothesis that enhanced memory associated with emotional experiences involves activation of the β-adrenergic system.
Hormonal mediation of the memory disorder in depression
The cognitive and mood effects of stimulant compounds in normal and depressed patient populations and parallels between the biologic and cognitive changes seen in normal aging and those observed in depression are considered.
Physiological Elevations of Glucocorticoids Potentiate Glutamate Accumulation in the Hippocampus
Examination of the effects of GCs over the normal physiological range on glutamate and aspartate profiles shows that the highly elevated GC concentrations that accompany neurological insults such as seizure or hypoxia‐ischemia will greatly exacerbate the glutamate accumulation at that time.
Rapid Communication: Adrenalectomy Attenuates Stress‐Induced Elevations in Extracellular Glutamate Concentrations in the Hippocampus
It is suggested that glucocorticoid‐in‐duced elevations in extracellular glutamate concentrations may contribute to the deleterious effects of stress on hippocampal neurons.
Control of neuronal excitability by corticosteroid hormones