We have previously demonstrated that acute treatment with low dose methamphetamine is neuroprotectivein a rat model of severe traumatic brain injury (TBI). Using gene expression analysis, we further showed that metham...We have previously demonstrated that acute treatment with low dose methamphetamine is neuroprotectivein a rat model of severe traumatic brain injury (TBI). Using gene expression analysis, we further showed that methamphetamine treatment significantly reduced the expression of pro-inflammatory genes after severe TBI. Therefore, to further investigate the potential effects of methamphetamine treatment on the neuroinflammatory response, we examined immunofluorescent staining of Iba1 and CD68, two marker of neuroinflammation, in the rat lateral fluid percussion injury model of severe TBI. In this study, we observed temporal and spatial alterations in the pattern of Iba1 and CD68 labeling within two weeks after severe TBI. In general, methamphetamine treatment did not dramatically alter the pattern of Iba1 and CD68 staining. However, we did observe a unique and significant drug-induced increase of Iba1 labeling within the granule cell layer of the dentate gyrusat 48 hours post injury. We also observed rod-shaped Iba1+?cells within the core lesion in the cortex. These cells showed variable staining with CD68 and aligned most closely with MAP2+?neuronal processes. Thus, acute treatment with low-dose methamphetamine after severe TBI caused a transient bilateral increase of Iba1+?cells within the granule layer of the dentate gyrus but did not alter the overall temporal and regional pattern of Iba1 and CD68 staining within the cortex, periventricular white matter, fimbria, or thalamus.展开更多
文摘We have previously demonstrated that acute treatment with low dose methamphetamine is neuroprotectivein a rat model of severe traumatic brain injury (TBI). Using gene expression analysis, we further showed that methamphetamine treatment significantly reduced the expression of pro-inflammatory genes after severe TBI. Therefore, to further investigate the potential effects of methamphetamine treatment on the neuroinflammatory response, we examined immunofluorescent staining of Iba1 and CD68, two marker of neuroinflammation, in the rat lateral fluid percussion injury model of severe TBI. In this study, we observed temporal and spatial alterations in the pattern of Iba1 and CD68 labeling within two weeks after severe TBI. In general, methamphetamine treatment did not dramatically alter the pattern of Iba1 and CD68 staining. However, we did observe a unique and significant drug-induced increase of Iba1 labeling within the granule cell layer of the dentate gyrusat 48 hours post injury. We also observed rod-shaped Iba1+?cells within the core lesion in the cortex. These cells showed variable staining with CD68 and aligned most closely with MAP2+?neuronal processes. Thus, acute treatment with low-dose methamphetamine after severe TBI caused a transient bilateral increase of Iba1+?cells within the granule layer of the dentate gyrus but did not alter the overall temporal and regional pattern of Iba1 and CD68 staining within the cortex, periventricular white matter, fimbria, or thalamus.
