Abstract
The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP− cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2−/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.
Highlights
The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear
The step-through latencies in the passive-avoidance test in the CO rats were significantly shorter than in the controls on day 7 (300.0 ± 0.0 vs. 269.2 ± 12.8, p = 0.029), day 14 (294.8 ± 5.0 vs. 236.0 ± 20.5, p = 0.036), and day 21 (296.6 ± 3.4 vs. 229.0 ± 22.4, respectively, p = 0.013) after CO poisoning (Fig. 1). These results suggest that the procedure of CO exposure induced delayed cognitive impairment in the rats and may be applicable as a model of delayed CO encephalopathy
This study demonstrated the delayed effects of CO exposure on neural precursor cells and glial cells in the adult dentate gyrus (DG) using our rat model to elucidate the pathophysiology of delayed CO encephalopathy
Summary
The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Rats exposed to CO (1000 ppm CO for 40 min and 3000 ppm for 20 min) showed time-dependent degradation of myelin basic protein and altered numbers of lymphocytes and microglia in the b rain[10] These results are insufficient to explain the pathophysiology of delayed CO encephalopathy. Previous studies including ours showed that the number of microglial cells and the level of glial fibrillary acidic protein (GFAP), a marker of astrocytes, are decreased 7 days after CO e xposure[16,17] Both astrocytes and microglial cells play a role in hippocampal neurogenesis, even in adults[18,19]. This study investigated the effects of CO exposure on neural precursor cells and glial cells in the granular cell layer and subgranular zone in the adult DG 21 days after CO exposure to elucidate the pathophysiology of delayed CO encephalopathy
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