Neural Modulation of the Immune Response through the Benzodiazepine/GABA Receptor Chloride Ionophore Complex

摘要

This project examines the role of the benzodiazepine/GABA receptor chloride ionophore complex (Supramolecular Complex) in the control of immune functions. We have found that the suppression of allogeneic CTL response by the benzodiazepine receptor inverse agonist, FG 7142 is dose-dependent, and that this suppression is long lasting. FG 7142 suppressed CTL response in male mice only, suggesting that the FG 7142-induced immune suppression may by sexually dimorphic. Natural Killer (NK) cell activity was also suppressed 2 hr after administration of FG 7142 and was still manifest 24 hr later. A profound suppression of immune functions (CTL, NK, and MLR responses) was also observed 2 hr after administration of a single dose of Alprazolam (a triazolbenzodiazepine with high affinity for 'central' but not 'peripheral' benzodiazepine receptors). These results suggest that the benzodiazepine receptors and the pathways subserved by these receptors may be important in the neural control of immunity. Keywords: Immunochemistry, Benzodiazepine receptors, B-Carbolines, Immunity, NK activity, Mitogen stimulation, T cells, Stress, Neuroimmunomodulation, CNS Cytotoxic T Lympocyte (CTL). (kt)