Acute stress induced modifications of calcium signaling in learned helpless rats
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 107231
Author(s) Velbinger, K; De Vry, J; Jentzsch, K; Eckert, A; Henn, F; Müller, W E
Author(s) at UniBasel Eckert, Anne
Year 2000
Title Acute stress induced modifications of calcium signaling in learned helpless rats
Journal Pharmacopsychiatry
Volume 33
Number 4
Pages / Article-Number 132-7
Abstract

Previous reports have demonstrated reduced elevations of free intracellular calcium concentration in blood cells of depressed patients after various stimuli. Therefore, a disturbance of intracellular calcium (Ca2+) homeostasis has been postulated to be involved in the pathophysiology of mood disorders. It was the aim of the present study to investigate whether Ca2+ signaling was affected in spleen T-lymphocytes of rats submitted to a learned helplessness paradigm, an animal model of depression with a high level of construct, face and predictive validity. In addition, we tested for effects of acute stress on the Ca2+ signaling in helpless rats, as compared to non-stressed rats. It was found that mitogen-induced Ca2+ signaling only tended to be reduced in helpless rats. However, when helpless rats were submitted to acute immobilization stress, Ca2+ signaling appeared to be significantly blunted, whereas the same stressor did not affect Ca2+ signaling in the non-helpless control rats. These acute stress-induced differences in Ca2+ signaling were not paralleled by a differential increase in plasma corticosterone. It is hypothesized that blunted Ca2+ signaling, as assessed in spleen T-lymphocytes of helpless rats, may be a correlate of the increased vulnerability of helpless rats to acute stressors.

Publisher Thieme
ISSN/ISBN 0720-4280
edoc-URL http://edoc.unibas.ch/dok/A5253498
Full Text on edoc No
Digital Object Identifier DOI 10.1055/s-2000-11220
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/10958261
ISI-Number WOS:000088643700002
Document type (ISI) Journal Article
 
   

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