TNFRSF1A and bipolar disorder: - Activates phagocytosis, proliferation, adhesion; promotes apoptosis of foreign cells (T93) - Modulates synaptic transmission and receptor localization; inhibits synaptic plasticity (T94) - Via TNFR1 enhances excitability by reducing GABA-A receptors (T95, T96) - Promotes AMPAR expression in cortex, increasing excitability (T54, T96) - May contribute to schizophrenia and bipolar depression (T95) - Increased in multiple sclerosis and models (T97)