Altered Postsynaptic-Density-Levels of Caldendrin in the Para-Chloroamphetamine-Induced Serotonin Syndrome but not in the Rat Ketamine Model of Psychosis |
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Authors: | Karl-Heinz Smalla Jale Sahin Jörg Putzke Wolfgang Tischmeyer Eckart D. Gundelfinger Michael R. Kreutz |
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Affiliation: | (1) Special Lab Molecular Biological Techniques, Leibniz-Institute for Neurobiology, Magdeburg, Germany;(2) Project Group Neuroplasticity, Leibniz-Institute for Neurobiology, Brenneckestr. 6, 39118 Magdeburg, Germany;(3) Institute of Medical Neurobiology, O-v-G University, Magdeburg, Germany;(4) Department of Neurochemistry and Molecular Biology, Leibniz-Institute for Neurobiology, Magdeburg, Germany;(5) Present address: Pfizer Limited, Sandwich, UK |
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Abstract: | Caldendrin is a synaptic calcium sensor protein that is tightly associated with the postsynaptic density (PSD). Previous work has shown that the association of the protein with the synapse is highly dynamic and is increased in an activity-dependent manner. In the present study the caldendrin-association with the postsynaptic cytomatrix was analyzed in animal models of psychosis and drug abuse induced neurotoxicity. Subchronic administration of the N-methyl-d-aspartate (NMDA)-receptor antagonist ketamine, serving as a model of NMDA-receptor hypofunction and schizophrenia showed no significant effect on the PSD-levels of caldendrin, indicating that NMDA-receptor activity is not required to keep caldendrin at the synapse. However, administration of high doses of the serotonergic neurotoxin p-chloroamphetamine (PCA) lead to significant changes in the association of caldendrin with the PSD. These results underscore the dynamic association of caldendrin with the PSD and suggest a role of this synaptic calcium sensor in the PCA-induced serotonin syndrome. |
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Keywords: | Caldendrin Ketamin-induced psychosis Psychotropic compounds Postsynaptic density p-Chloroamphetamine-induced serotonin syndrome |
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