Abstract
Exposure to stressful events has profound impact on hippocampus-dependent learning and memory processes. Traumatic and stressful experiences are remembered well in general, but have also been reported to suppress learning and memory processes. These bi-directional effects are, at least in part, modulated by corticosteroid hormones that are released during exposure to stressful experiences. An important question that remains to be addressed is how exactly exposure to stressful situations and elevated corticosteroid hormone levels affect learning and memory processes. Evidence is accumulating that exposure to stressful situations and elevated corticosteroid hormone levels modulates fast excitatory amino acid mediated synaptic transmission and synaptic plasticity, which are considered to underlie learning and memory processes in the hippocampus. In particular, exposure to stressful events has been reported to facilitate synaptic plasticity when delivered shortly before or after high frequency stimulation. By contrast, stressful events and elevated corticosteroid hormones suppress synaptic potentiation when stress precedes high frequency stimulation. From the mechanistic point of view, it is potentially important that exposure to stressful events and elevated corticosteroid hormone levels target key mechanisms that are involved in synaptic plasticity, i.e. AMPA receptors and NMDA receptors.
Keywords: corticosterone, mineralocorticoid receptor (MR), AMPA receptor, CA1 area, synaptic plasticity
CNS & Neurological Disorders - Drug Targets
Title: Stress, Corticosteroid Hormones and Hippocampal Synaptic Function
Volume: 5 Issue: 5
Author(s): Deborah N. Alfarez, Olof Wiegert and Harm J. Krugers
Affiliation:
Keywords: corticosterone, mineralocorticoid receptor (MR), AMPA receptor, CA1 area, synaptic plasticity
Abstract: Exposure to stressful events has profound impact on hippocampus-dependent learning and memory processes. Traumatic and stressful experiences are remembered well in general, but have also been reported to suppress learning and memory processes. These bi-directional effects are, at least in part, modulated by corticosteroid hormones that are released during exposure to stressful experiences. An important question that remains to be addressed is how exactly exposure to stressful situations and elevated corticosteroid hormone levels affect learning and memory processes. Evidence is accumulating that exposure to stressful situations and elevated corticosteroid hormone levels modulates fast excitatory amino acid mediated synaptic transmission and synaptic plasticity, which are considered to underlie learning and memory processes in the hippocampus. In particular, exposure to stressful events has been reported to facilitate synaptic plasticity when delivered shortly before or after high frequency stimulation. By contrast, stressful events and elevated corticosteroid hormones suppress synaptic potentiation when stress precedes high frequency stimulation. From the mechanistic point of view, it is potentially important that exposure to stressful events and elevated corticosteroid hormone levels target key mechanisms that are involved in synaptic plasticity, i.e. AMPA receptors and NMDA receptors.
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Cite this article as:
Alfarez N. Deborah, Wiegert Olof and Krugers J. Harm, Stress, Corticosteroid Hormones and Hippocampal Synaptic Function, CNS & Neurological Disorders - Drug Targets 2006; 5 (5) . https://dx.doi.org/10.2174/187152706778559345
DOI https://dx.doi.org/10.2174/187152706778559345 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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