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          Institute: MPI für medizinische Forschung     Collection: jahrbuch_2011_archival     Display Documents

ID: 597820.0, MPI für medizinische Forschung / jahrbuch_2011_archival
AMPA GluR−A Receptor Subunit Mediates Hippocampal
Responsiveness in Mice Exposed to Stress
Translation of Title:AMPA GluR−A Receptor Subunit Mediates Hippocampal
Responsiveness in Mice Exposed to Stress
Authors:Fumagalli, Fabio; Caffino, Lucia; Vogt, Miriam A.; Frasca, Angelisa; Racagni, Giorgio; Sprengel, Rolf; Gass, Peter; Riva, Marco Andrea
Date of Publication (YYYY-MM-DD):2011-09-01
Title of Journal:Hippocampus
Journal Abbrev.:Hippocampus
Issue / Number:9
Start Page:1028
End Page:1035
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description:Because stress represents a major recipitating event for psychiatric disorders, it is important to identify molecular mechanisms that may be altered in vulnerable individuals when exposed to stress.
Here, we studied GluR−A2/2 mice, animals with compromised AMPA receptor signaling, and characterized by a schizophrenic as well as
depressive phenotype to investigate changes occurring in response to an
acute stress. Wild−type and GluR−A2/2 mice were exposed to a single
immobilization stress and sacrificed immediately after the end of the
stress for the analysis of activity regulated genes and of glutamatergic
synapse responsiveness. The acute stress produced a marked increase in
the hippocampal expression of Arc (activity−regulated cytoskeletal−associated
protein) in GluR−A2/2, but not in wild−type mice, which was
associated with a similar increase of phospho−CaMKII, a partner in the
action of Arc. When looking at the glutamatergic response to stress in
wild−type animals, we found that stress increased GluR−A phosphorylation
on serine831, an effect that was paralleled by a significant increase
of the phosphorylation of the main NMDA receptor subunits, that is,
NR−1 and NR−2B. Conversely, the stress−induced modulation of NMDA
receptor subunits was not observed in GluR−A2/2 mice. We suggest that
enhanced stress responsiveness in GluR−A2/2 mice may be due, at least
in part, to their inability to activate NMDA−mediated glutamatergic neurotransmission,
suggesting that the integrity of AMPA/NMDA receptor
function may be important for successful coping under stressful conditions
Free Keywords:glutamate ; NMDA receptors ; activity regulated cytoskeletal−associated protein ; CaMKII ; glucocorticoids ; synapsin I
External Publication Status:published
Document Type:Article
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie
MPI für medizinische Forschung/Abteilung Zellphysiologie/Olfaction Web
MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie/Gruppe Rolf Sprengel
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