Effects of D2-dopamine and alpha-adrenoceptor antagonists in stress induced changes on immune responsiveness of mice
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12225888
DOI
10.1016/s0165-5728(02)00211-4
PII: S0165572802002114
Knihovny.cz E-resources
- MeSH
- Adrenergic alpha-Antagonists pharmacology MeSH
- Receptors, Adrenergic, alpha drug effects immunology MeSH
- Dopamine D2 Receptor Antagonists MeSH
- Dopamine Antagonists pharmacology MeSH
- B-Lymphocytes cytology immunology MeSH
- Killer Cells, Natural cytology immunology MeSH
- Phenotype MeSH
- Stress, Physiological immunology metabolism physiopathology MeSH
- Immune System drug effects immunology MeSH
- Catecholamines immunology MeSH
- Leukocytes, Mononuclear cytology drug effects immunology MeSH
- Brain drug effects immunology metabolism MeSH
- Mice, Inbred CBA MeSH
- Mice MeSH
- Neuroimmunomodulation drug effects immunology MeSH
- Neurosecretory Systems drug effects immunology MeSH
- GTP-Binding Proteins immunology MeSH
- Receptors, Dopamine D2 immunology MeSH
- Spleen cytology drug effects immunology MeSH
- T-Lymphocytes cytology immunology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adrenergic alpha-Antagonists MeSH
- Receptors, Adrenergic, alpha MeSH
- Dopamine D2 Receptor Antagonists MeSH
- Dopamine Antagonists MeSH
- Catecholamines MeSH
- GTP-Binding Proteins MeSH
- Receptors, Dopamine D2 MeSH
The involvement of catecholamine receptors (alpha-adrenergic, D2-dopamine (DA)) was investigated in restraint stress influenced immune responses with concomitant changes of G-protein signal transduction. Impairment of the spleen morphology, TH1/TH2 cytokine network and natural killer (NK) cell function was observed. In vivo administration of specific antagonists prior to restraint stress reversed the immunosuppression. These findings demonstrate that D2-type dopaminergic mechanism represents the dominant component in regulation of Galphas/Galphai(1,2)/Galphaq/11-protein signal transduction and contribute to cell responses at postreceptor level of both, central nervous and immune systems. G-protein-coupled receptors (GPCRs) can modulate cytokine production and may play a regulatory role in immune effector mechanisms.
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