Journal
BRAIN
Volume 136, Issue -, Pages 3753-3765Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/awt293
Keywords
long-term potentiation; metaplasticity; glucocorticoids; glutamate receptor; calcium
Categories
Funding
- BBSRC
- WCU Programme (Korea)
- UK Wellcome Trust-Medical Research Council Neurodegenerative Disease Initiative Programme
- Korea-UK Alzheimer's disease Research Consortium Programme (the Korean Ministry of Health and Welfare)
- Frontier Programme in Neuroscience (Korea)
- Chonnam National University Hospital Frontier Lab Programme for Translational Neuroscience
- Department for Business, Innovation and Skill GFP program (UK)
- Wolfson Research Merit Award
- Royal Society, London
- BBSRC [BB/G00403X/1] Funding Source: UKRI
- MRC [MC_G1000734, MR/K023098/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G00403X/1] Funding Source: researchfish
- Medical Research Council [MC_G1000734, MR/K023098/1, 983724] Funding Source: researchfish
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The neuroendocrine response to episodes of acute stress is crucial for survival whereas the prolonged response to chronic stress can be detrimental. Learning and memory are particularly susceptible to stress with cognitive deficits being well characterized consequences of chronic stress. Although there is good evidence that acute stress can enhance cognitive performance, the mechanism(s) for this are unclear. We find that hippocampal slices, either prepared from rats following 30 min restraint stress or directly exposed to glucocorticoids, exhibit an N-methyl-D-aspartic acid receptor-independent form of long-term potentiation. We demonstrate that the mechanism involves an NMDA receptor and PKA-dependent insertion of Ca2+-permeable AMPA receptors into synapses. These then trigger the additional NMDA receptor-independent form of LTP during high frequency stimulation.
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