Spontaneous reactive astrogliosis in the dentate gyrus of Bax-deficient mice

Abstract

Astrocytes play critical roles in many aspects of brain functions via modulation of neurotransmission, metabolism, 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 Baxknockout mice may play a role in tissue remodeling of the dentate gyrus following a failure in the programmed cell death of adult-produced neurons.