Article date: 1992/11/1
PubMed ID: 1339052
Journal name: The International journal of neuroscience (ISSN: 0020-7454)
Participation of a GABA-ergic system in neuroimmunomodulation was established through the use of a large number of chemical compounds which selectively modulate the activity of the GABA-BD-receptor-ionophore complex. Activation of the GABA-receptors with muscimol or activation of the BD-receptors with diazepam or tazepam had stimulatory effects upon immunogenesis. A decrease in the GABA-BD-receptor-ionophore complex activity led to a suppression of the immune response. The effect was achieved with: a blockade of the complex with bicuculline–a competitive inhibitor of the GABA-receptors: administration of a specific antagonist of the BD-receptors flumazenil or Ro 15-3505: or with blockade of chloride channels with picrotoxin. Activation of the GABA-ergic system causes an increase in bone marrow content of T-helper cells marked by L3T4. The immunomodulatory action of the GABA-ergic system is of central origin and can occur only when the hypothalamo-pituitary system is intact. Section of the pituitary stalk prevents accumulation of the T-helper cells in the bone marrow. The result show that the influence of GABA-ergic system on immunogenesis requires participation of both dopaminergic and serotoninergic systems.
Author List: Devoino L, Idova G, Beletskaya I
Publication Types: Journal Article
Substances mentioned in the article: Receptors, GABA-A; Serotonin; Dopamine;
Mesh terms: Animals; Dopamine/immunology; Female; Immune System/metabolism; Male; Mice; Neuroimmunomodulation; Phenotype; Receptors, GABA-A/immunology; Rosette Formation; Serotonin/immunology; T-Lymphocytes/immunology; T-Lymphocytes, Helper-Inducer/immunology;