Since a number of pre-clinical and clinical studies has confirmed a role of the hypothalamic-pituitary-adrenal axis, neurotrophins, and immune activation in the pathogenesis of depression and detrusor overactivity, we wanted to know whether activation of GPR55 receptors is able to abolish the corticosterone-induced disturbances in the urine and/or the hippocampus levels of IL-1β, TNF-α, CRF, BDNF, and NGF in female rats. The gene discussed is BDNF; the disease is depressive disorder.