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Altered postsynaptic-density-levels of caldendrin in the para-chloroamphetamine-induced serotonin syndrome but not in the rat ketamine model of psychosis.

Authors: Smalla, Karl-Heinz  Sahin, Jale  Putzke, Jörg  Tischmeyer, Wolfgang  Gundelfinger, Eckart D  Kreutz, Michael R 
Citation: Smalla KH, etal., Neurochem Res. 2009 Aug;34(8):1405-9. doi: 10.1007/s11064-009-9925-8. Epub 2009 Feb 18.
Pubmed: (View Article at PubMed) PMID:19224364
DOI: Full-text: DOI:10.1007/s11064-009-9925-8

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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RGD Object Information
RGD ID: 14399959
Created: 2019-05-07
Species: All species
Last Modified: 2019-05-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.