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Biotinylated dextran amine is an ideal anterograde tracer for the corticospinal tract in a goat model of ischemic corticospinal tract injury

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Neural Regeneration Research 2011年第25期6卷 1960-1964页

作者： Xiaoyu Yang Yufei Gao Zhigang Qin Xia Cao Xinquan Gu China-Japan Union Hospital Jifin University Changchun 130033 Jilin Province China School of Pharmaceutical Sciences Jilin University Changchun 130021 Jifin Province China

Existing visualized tracer studies of the corticospinal tract have been focused on rodents, which have markedly different spinal cord structures compared with humans. In this study, the segmental artery feeding the spinal cord was embolized with digital subtraction angiography to establish a goat model of ischemic spinal cord injury. Biotinylated dextran amine was injected into the motor function areas of the cortex in goats with ischemic spinal cord injury. The corticospinal tract originates from the cerebral cortex motor function area, and travels towards the lateral funiculus at the contralateral spinal dorsal horn after decussation at the pyramid. The number of corticospinal tract positive fibers was found to be gradually reduced. These findings indicate that digital subtraction angiography can be applied to a goat model of ischemic spinal cord injury. Biotinylated dextran amine visualizes the course of the goat corticospinal tract in the spinal cord, which is similar to the human spinal cord. Biotinylated dextran amine is an ideal tracer for the corticospinal tract.

关键词： corticospinal tract biotinylated dextran amine ischemic spinal cord injury digital subtraction angiography tracer neuroanatomy neural regeneration

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Serine-threonine protein kinase activation may be an effective target for reducing neuronal apoptosis after spinal cord injury

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Neural Regeneration Research 2015年第11期10卷 1830-1835页

作者： Mu Jin Yan-wei Yang Wei-ping Cheng Jia-kai Lu Si-yu Hou Xiu-hua Dong Shi-yao Liu Department of Anesthesiology Beijing Anzhen Hospital Capital Medical University Beijing Institute of Heart Lung and Blood Vessel Diseases

The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood. We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury, including extracellular signal-regulated kinase（ERK）, serine-threonine protein kinase（Akt） and c-Jun N-terminal kinase（JNK） signaling pathways. We established a rat model of acute spinal cord injury by inserting a catheter balloon in the left subclavian artery for 25 minutes. Rat models exhibited notable hindlimb dysfunction. Apoptotic cells were abundant in the anterior horn and central canal of the spinal cord. The number of apoptotic neurons was highest 48 hours post injury. The expression of phosphorylated Akt（pAkt） and phosphorylated ERK（p-ERK） increased immediately after reperfusion, peaked at 4 hours（p-Akt） or 2 hours（p-ERK）, decreased at 12 hours, and then increased at 24 hours. Phosphorylated JNK expression reduced after reperfusion, increased at 12 hours to near normal levels, and then showed a downward trend at 24 hours. Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression. These findings suggest that activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia, particularly at the stage of reperfusion, and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.

关键词： nerve regeneration ischemic spinal cord injury cell apoptosis neurological function serine-threonine protein kinase extracellular signal-regulated kinase c-Jun N-terminal kinase neural regeneration

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