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Eye Tracking, Cortisol, and a Sleep vs. Wake Consolidation Delay: Combining Methods to Uncover an Interactive Effect of Sleep and Cortisol on Memory
Published on: June 18, 2014
Temporal modulation of hippocampal excitatory transmission by corticosteroids and stress
Francis Chaouloff1, Laurent Groc
1Endocannabinoïdes et NeuroAdaptation, NeuroCentre Magendie INSERM U862, Bordeaux, France. francis.chaouloff@inserm.fr
Abstract:
There is overwhelming evidence for multiple effects of stress on excitatory transmission and synaptic plasticity in the hippocampus. These interactions between stress and hippocampal glutamatergic neurons play a role in the cognitive and emotional consequences of aversive stimuli. Stress impacts on excitatory synapses are mediated by a complex set of neurohormones and neurotransmitters, among which corticosteroid hormones secreted from the adrenal cortex play a crucial role. Most effects of corticosteroid hormones are mediated by their binding to cytosolic mineralocorticoid (MR) and glucocorticoid receptors (GR), which after translocation to the nucleus, regulate the transcription of target genes. Recent electrophysiological and live imaging experiments have however provided experimental data which reinforce the hypothesis that beside these delayed effects, corticosteroid hormones may also act rapidly through membrane receptors. The first goal of this review is to detail the tonic and intrinsic effects of corticosteroid hormones on hippocampal excitatory transmission, glutamate receptor trafficking and expression, and synaptic plasticity, paying attention to their temporality (rapid and transient effects followed by slow and persistent genomic effects). Its second goal is to dissect the extent to which acute/repeated stress influences hippocampal excitatory synapses and whether these are accounted for by corticosteroid hormones.
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