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Alterations of signal transduction in lymphocytes cultured from patients with bipolar disorder

Bipolar disorder is a psychiatric condition which affects up to 1% of the general population and results in episodes of mania and depression. Molecular biological studies have shown that several components of the signal transduction pathways are affected in bipolar illness. However, the precise systems and components involved in the disorder still remain unknown. Our goal was to identify some of the differences in signal transduction pathways of B-lymphocytes. Using cultured lymphocytes obtained from bipolar patients, we found that there exist no difference in the levels of protein kinase C, Galphas and Galphai proteins, and tubulin between control and bipolar cell lines following stimulation of the PI pathway with the 5-HT 2 receptor agonist, alpha-methyl serotonin. These data are not consistent with previous findings. The lack of a significant difference between control and bipolar with respect to PKC might be due to the fact that we studied a different cell type or to poor stimulation conditions, and/or possibly to a high PKC content in the membrane of these cells, thereby masking the effect of stimulation. The results obtained for the G proteins can be attributed to a lack of effect of the agonist on these proteins which are associated with the adenylate cyclase pathway.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.33738
Date January 2001
CreatorsConstant, Peggy.
ContributorsPalmour, Roberta (advisor)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageMaster of Science (Department of Biology.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001872215, proquestno: MQ78855, Theses scanned by UMI/ProQuest.

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