geranylgeranylacetone and staurosporine-aglycone

Heat shock proteins (HSPs) are stress-induced chaperones that are involved in neurological disease. Although increasingly implicated in behavioral disorders, the mechanisms of HSP action, and the relevant functional pathways, are still unclear. We examined whether oral administration of geranylgeranylacetone (GGA), a known HSP inducer, produced an antidepressant effect in a social defeat stress model of depression in mice. We also investigated the possible molecular mechanisms involved, particularly focusing on hippocampal neurogenesis and neurotrophic factor expression. In stressed mice, hippocampal HSP105 expression decreased. However, administration of GGA increased HSP105 expression and improved depression-like behavior, induced hippocampal cell proliferation, and elevated brain-derived neurotrophic factor (BDNF) levels in mouse hippocampus. Co-treatment with GGA and the BDNF receptor inhibitor K252a suppressed the antidepressant effects of GGA. HSP105 knockdown decreased

Topics: Animals; Behavior, Animal; Brain-Derived Neurotrophic Factor; Carbazoles; Cell Line; Depression; Diterpenes; Gene Expression Regulation; Hippocampus; HSP110 Heat-Shock Proteins; Indole Alkaloids; Male; Mice; Receptor, trkB; Stress, Psychological