Astrocytes play critical roles in many aspects of brain functions via modulation of neurotransmission, metabol-ism, and structural remodeling in response to physiological or pathological stimuli. Activation of astrocytes is a common phenomenon in many brain pathologies such as stroke, trauma, and neurodegenerative diseases. In this study, we found that gene deletion of the pro-apoptotic gene Bax (Bax-knockout) resulted in a spontaneous reactive astrogliosis in the dentate gyrus, as evidenced by the increased number/volume of astrocytes and cytoplasmic localization of the Olig2 protein. On the other hand, there was no evidence for microglial activation in the dentate gyrus of Bax-knockout mice. Previously, we reported that Bax-knockout mice failed to execute programmed cell death of adult-produced neurons, but the surplus neurons eventually impaired normal synaptic connections and dendritic arborization of dentate gyrus neurons. Therefore, we propose that the reactive astrocytes in the Bax-knockout mice may play a role in tissue remodeling of the dentate gyrus following a failure in the programmed cell death of adult-produced neurons.

Keywords: astrogliosis, Bax, microglial activation, neurogenesis, progrmmed cell death