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Corticosterone alters AMPAR mobility and facilitates bidirectional synaptic plasticity
- Source :
- PLoS ONE, 4(3):e4714. Public Library of Science, PLoS ONE, Vol 4, Iss 3, p e4714 (2009), PLoS ONE, PLoS ONE, Public Library of Science, 2009, 4 (3), pp.e4714. ⟨10.1371/journal.pone.0004714⟩, PLoS One (print), 4(3). Public Library of Science
- Publication Year :
- 2009
-
Abstract
- International audience; BACKGROUND: The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the bidirectional effects of stress and corticosteroid hormones on synaptic efficacy and learning and memory processes. In this study we investigate the relationship between corticosterone and AMPA receptors which play a critical role in activity-dependent plasticity and hippocampal-dependent learning. METHODOLOGY/PRINCIPAL FINDINGS: Using immunocytochemistry and live cell imaging techniques we show that corticosterone selectively increases surface expression of the AMPAR subunit GluR2 in primary hippocampal cultures via a glucocorticoid receptor and protein synthesis dependent mechanism. In agreement, we report that corticosterone also dramatically increases the fraction of surface expressed GluR2 that undergo lateral diffusion. Furthermore, our data indicate that corticosterone facilitates NMDAR-invoked endocytosis of both synaptic and extra-synaptic GluR2 under conditions that weaken synaptic transmission. CONCLUSION/SIGNIFICANCE: Our results reveal that corticosterone increases mobile GluR2 containing AMPARs. The enhanced lateral diffusion properties can both facilitate the recruitment of AMPARs but under appropriate conditions facilitate the loss of synaptic AMPARs (LTD). These actions may underlie both the facilitating and suppressive effects of corticosteroid hormones on synaptic plasticity and learning and memory and suggest that these hormones accentuate synaptic efficacy.
- Subjects :
- MESH: Hippocampus
MESH: Receptors, Glucocorticoid
Anti-Inflammatory Agents
MESH: Neurons
Nonsynaptic plasticity
lcsh:Medicine
Hippocampus
Synaptic Transmission
chemistry.chemical_compound
0302 clinical medicine
Corticosterone
MESH: Animals
MESH: Neuronal Plasticity
lcsh:Science
Neurons
0303 health sciences
Neuronal Plasticity
Neuroscience/Behavioral Neuroscience
MESH: Electrophysiology
Multidisciplinary
Synaptic scaling
Neuroscience/Animal Cognition
Endocytosis
Electrophysiology
MESH: N-Methylaspartate
MESH: Adaptor Protein Complex 2
MESH: Receptors, AMPA
MESH: Endocytosis
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
Fluorescence Recovery After Photobleaching
Research Article
medicine.medical_specialty
N-Methylaspartate
MESH: Rats
Adaptor Protein Complex 2
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
AMPA receptor
Biology
03 medical and health sciences
Receptors, Glucocorticoid
Internal medicine
Synaptic augmentation
Metaplasticity
Neuroscience/Neuronal Signaling Mechanisms
MESH: Synaptic Transmission
medicine
Animals
[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology
Receptors, AMPA
030304 developmental biology
lcsh:R
Rats
Endocrinology
Synaptic fatigue
chemistry
nervous system
MESH: Anti-Inflammatory Agents
Synaptic plasticity
lcsh:Q
MESH: Corticosterone
Neuroscience
MESH: Fluorescence Recovery After Photobleaching
030217 neurology & neurosurgery
Subjects
Details
- Language :
- English
- ISSN :
- 19326203
- Database :
- OpenAIRE
- Journal :
- PLoS ONE, 4(3):e4714. Public Library of Science, PLoS ONE, Vol 4, Iss 3, p e4714 (2009), PLoS ONE, PLoS ONE, Public Library of Science, 2009, 4 (3), pp.e4714. ⟨10.1371/journal.pone.0004714⟩, PLoS One (print), 4(3). Public Library of Science
- Accession number :
- edsair.doi.dedup.....a4aa710a97a171ef3a8bc5e0fd153fb8