Abstract
Ionizing radiation has become an inevitable health concern emanating from natural sources like space travel and from artificial sources like medical therapies. In general, exposure to ionizing radiation such as γ-rays is one of the methods currently used to stress specific model systems. In this study, we elucidated the long-term effect of acute and fractionated irradiation on DCX-positive cells in hippocampal neurogenesis. Groups of two-month-old C57BL/6 female mice were exposed to whole-body irradiation at acute dose (5 Gy) or fractional doses (1 Gy × 5 times and 0.5 Gy × 10 times). Six months after exposure to γ-irradiation, the hippocampus was analyzed. Doublecortin (DCX) immunohistochemistry was used to measure changes of neurogenesis in the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG). The number of DCX-positive cells was significantly decreased in all acute and fractionally irradiation groups. The long-term changes in DCX-positive cells triggered by radiation exposure showed a very different pattern to the short-term changes which tended to return to the control level in previous studies. Furthermore, the number of DCX-positive cells was relatively lower in the acute irradiation group than the fractional irradiation groups (approximately 3.6-fold), suggesting the biological change on hippocampal neurogenesis was more susceptible to being damaged by acute than fractional irradiation. These results suggest that the exposure to γ-irradiation as a long-term effect can trigger biological responses resulting in the inhibition of hippocampal neurogenesis.
Highlights
Neurodegeneration, the progressive loss of structure or function of neurons, results in many neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and Huntington’s [1,2,3,4]
Doublecortin (DCX) as a progenitor neural cell marker, a microtubule-associated phospho-protein, has been utilized for analyzing alterations in neurogenesis in the adult dentate gyrus (DG) because it is believed to be specific to neuronal antigens expressed by newly born neurons [8]
DCX immunoreactivity was relatively lower in the acute irradiation group than in the fractionated irradiation groups, but there was no significant difference in the fractionated irradiation (Figure 2B)
Summary
Neurodegeneration, the progressive loss of structure or function of neurons, results in many neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and Huntington’s [1,2,3,4]. Even though the risk to radiation exposure in the brain is a big issue, the changes in the hippocampal neurodegeneration are poorly understood. The risk of short-term neurodegeneration caused by radiation exposure has been reported [17,18,19,20,21,22]. Kim’s group suggested that transient impairment of the functioning of the hippocampus is linked to inhibition of hippocampal neurogenesis after acute γ-irradiation [9]. The Abdallah group reported that irradiation can reversibly alter proliferation, neurogenesis, and cell death in the dentate gyrus of adult mice. We hypothesized that the long-term changes in DCX-positive cells caused by γ-irradiation would continuously increase neurodegeneration resulting in damage to the hippocampal function as opposed to the recovering tendency of neurogenesis impairment in the short term. Understanding how irradiation affects neurogenesis may provide useful insight into potential approaches to reduce brain-related diseases
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