Neuronal proteins involved in synaptic targeting of AMPA receptors in rat hippocampus by antidepressant drugs

Recent data suggest that the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor subtype plays a pivotal role in the pathogenesis of effective disorders and in the action of antidepressant drugs. After chronic treatment with the antidepressants desipramine or paroxetine, w...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-02, Vol.353 (3), p.750-755
Main Authors: Martínez-Turrillas, Rebeca, Del Río, Joaquín, Frechilla, Diana
Format: Article
Language:English
Subjects:
AMPA receptors
Animals
Antidepressants
Antidepressive Agents - pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases - physiology
Desipramine - pharmacology
Glutamate
Hippocampus
Hippocampus - physiology
Male
Mood disorders
Neuronal Plasticity - physiology
Paroxetine - pharmacology
Protein Subunits - drug effects
Protein Subunits - metabolism
Protein Transport
Rats
Rats, Wistar
Receptors, AMPA - drug effects
Receptors, AMPA - physiology
Synapses - physiology
Synaptic plasticity
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Recent data suggest that the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor subtype plays a pivotal role in the pathogenesis of effective disorders and in the action of antidepressant drugs. After chronic treatment with the antidepressants desipramine or paroxetine, we measured by immunoprecipitation and Western blotting, the changes in the interaction of AMPA receptor subunits with proteins involved in trafficking and/or stabilization of the subunits into synaptic membranes of the hippocampus. Both antidepressants increased the interaction of GluR1 subunit with stargazin and of GluR2/3 with NSF. Paroxetine increased the interaction of GluR1 with Rab4A, and desipramine markedly increased the interaction of GluR1 with SAP97. Paroxetine, but not desipramine, also increased membrane levels of CaMKII, autophosphorylated CaMKII and GluR1 phosphorylated at the CaMKII site. Interactions of GluR1 and GluR2/3 with proteins implicated in AMPA receptor trafficking and with scaffolding proteins appear to account for the enhanced membrane expression of AMPA receptors in the hippocampus after antidepressant treatment.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.12.078