Furthermore, administration of IL-1β (5 μg/kg, 1 μL per side) into DG abolished the increased number of BrdU+Sox2+GFAP+ RGLs, BrdU+DCX+ neuroblasts, and BrdU+NeuN+ newborn neurons in DG by COS treatment of CRS-exposed mice (Fig. 5f, g), indicating that IL-1β abrogates the protective effect on AHN deficits in DG under chronic stress after COS treatment. The gene discussed is GFAP; the disease is congenital rubella syndrome.