Stress by noise produces differential effects on the proliferation rate of radial astrocytes and survival of neuroblasts in the adult subgranular zone.

The subgranular zone (SGZ) in the dentate gyrus contains radial astrocytes, known as Type-1 or Type-B cells, which generate neuroblasts (Type-2 cells or Type-D cells) that give rise to granular neurons. Stress increases glucocorticoid levels that target SGZ and modify the proliferation and apoptosis of hippocampal cells. Yet, it is not well-known whether stress differentially affects SGZ progenitors. We investigated the effects of noise-induced stress on the rate of proliferation and apoptosis of the Type-1 cells, Type-2 cells and newly generated granular neurons in the SGZ. We exposed Balb/C mice to noise using a standardized rodents' audiogram-fitted adaptation of a human noisy environment. We measured corticosterone serum levels at different time points. Animals received BrdU injections for 3 days and sequential sacrifices were done to carry out double-immunohistochemical analyses. We found that a 24-h noise exposure did not produce adaptative response in the curve of corticosterone as compared to a 12-h noise exposure. The percentage of BrdU+/GFAP+ cells was significantly reduced in the stress group as compared to controls. A high proportion of CASP-3+/GFAP+ radial astrocytes were found in the stress group. The percentage of BrdU+/doublecortin+ cells was higher in controls than in the stress group. Interestingly, the apoptosis rate of doublecortin-expressing cells in the stress group was slightly lesser than in controls. Remarkably, we did not find significant differences in the number of BrdU+/NeuN+ and CASP-3+/NeuN+ neurons. These data indicate that stress differentially affects the rate of proliferation and apoptosis in SGZ progenitors and suggest a possible compensatory mechanism to keep the net number of granular neurons.