Abstract:
: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.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Gonzalez-Perez O,Chavez-Casillas O,Jauregui-Huerta F,Lopez-Virgen V,Guzman-Muniz J,Moy-Lopez N,Gonzalez-Castaneda RE,Luquin Sdoi
10.1016/j.neures.2011.03.013subject
Has Abstractpub_date
2011-07-01 00:00:00pages
243-50issue
3eissn
0168-0102issn
1872-8111pii
S0168-0102(11)00101-5journal_volume
70pub_type
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