Neuronal proteins involved in synaptic targeting of AMPA receptors in rat hippocampus by antidepressant drugs
Autor: | Rebeca Martínez-Turrillas, Diana Frechilla, Joaquín Del Río |
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Rok vydání: | 2007 |
Předmět: |
Male
Biophysics Hippocampus AMPA receptor Pharmacology Biochemistry Ca2+/calmodulin-dependent protein kinase Desipramine medicine Animals Receptors AMPA Rats Wistar Long-term depression Molecular Biology Neuronal Plasticity Chemistry musculoskeletal neural and ocular physiology Glutamate receptor Cell Biology Antidepressive Agents Rats Paroxetine Protein Subunits Protein Transport nervous system Calcium-Calmodulin-Dependent Protein Kinases Synapses Synaptic plasticity Antidepressant Calcium-Calmodulin-Dependent Protein Kinase Type 2 medicine.drug |
Zdroj: | Biochemical and Biophysical Research Communications. 353:750-755 |
ISSN: | 0006-291X |
Popis: | 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. |
Databáze: | OpenAIRE |
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