The γ-aminobutyric acid neurotransmitter in the spinal cord dorsal horn plays an important role in pain modulation through primary afferent-mediated presynaptic inhibition. The weakening of γ-aminobutyric acid-media...The γ-aminobutyric acid neurotransmitter in the spinal cord dorsal horn plays an important role in pain modulation through primary afferent-mediated presynaptic inhibition. The weakening of γ-aminobutyric acid-mediated presynaptic inhibition may be an important cause of neuropathic pain. γ-aminobutyric acid-mediated presynaptic inhibition is related to the current strength of γ-aminobutyric acid A receptor activation. In view of this, the whole-cell patch-clamp technique was used here to record the change in muscimol activated current of dorsal root ganglion neurons in a chronic constriction injury model. Results found that damage in rat dorsal root ganglion neurons following application of muscimol caused concentration-dependent activation of current, and compared with the sham group, its current strength and γ-aminobutyric acid A receptor protein expression decreased. Immunofluorescence revealed that γ-aminobutyric acid type A receptor α2 subunit protein expression decreased and was most obvious at 12 and 15 days after modeling. Our experimental findings confirmed that the y-aminobutyric acid type A receptor α2 subunit in the chronic constriction injury model rat dorsal root ganglion was downregulated, which may be one of the reasons for the reduction of injury in dorsal root ganglion neurons following muscimol-activated currents.展开更多
To investigate the neurotoxicity of intrathecal injections of dexmedetomidine,Sprague-Dawley rats were intrathecally injected with dexmedetomidine at doses of 0.75,1.50 and 3.00μg/kg into the spinal dorsal horn.We fo...To investigate the neurotoxicity of intrathecal injections of dexmedetomidine,Sprague-Dawley rats were intrathecally injected with dexmedetomidine at doses of 0.75,1.50 and 3.00μg/kg into the spinal dorsal horn.We found that c-Fos expression in the rat spinal dorsal horn peaked at 7 hours following the 3.00μg/kg dexmedetomidine injection,while the levels of c-Fos expression following 0.75 and 1.50μg/kg dexmedetomidine were similar to those in the spinal dorsal horn of normal rats. At 48 hours following administration,the level of c-Fos expression was similar to normal levels.In addition,the intrathecal injections of dexmedetomidine increased paw withdrawal mechanical thresholds and prolonged thermal tail flick latencies.These results indicate that dexmedetomidine has pronounced antinociceptive effects.However,dexmedetomidine appears to have neurotoxic effects in the spinal cord because it increased c-Fos expression in the spinal dorsal horn within 7 hours following administration.展开更多
目的：研究自发性高血压大鼠降压前后的机械痛阈和热痛阈改变.方法：15只自发性高血压大鼠在实验 d 4～11肌注利血平注射液（1 μg·kg^-1·d^-1）.血压、机械刺激缩足反应阈值和热刺激缩足反应潜伏期作为观察指标.结果：自发...目的：研究自发性高血压大鼠降压前后的机械痛阈和热痛阈改变.方法：15只自发性高血压大鼠在实验 d 4～11肌注利血平注射液（1 μg·kg^-1·d^-1）.血压、机械刺激缩足反应阈值和热刺激缩足反应潜伏期作为观察指标.结果：自发性高血压大鼠经利血平降压治疗后血压明显下降约 50 mmHg 左右,机械痛阈和热痛阈均降低（P＜0.05）.结论：自发性高血压可能对自发性高血压大鼠的伤害性感受系统存在可逆的结构和（或）功能影响.展开更多
目的:药物治疗神经病理性疼痛的效果有限且不良反应多,而运动是治疗疼痛的一种较好的方式。文章系统性评价运动对大鼠、小鼠坐骨神经损伤诱发神经性疼痛的干预效果。方法:检索万方、中国知网、PubMed、Embase和Web of Science数据库,检...目的:药物治疗神经病理性疼痛的效果有限且不良反应多,而运动是治疗疼痛的一种较好的方式。文章系统性评价运动对大鼠、小鼠坐骨神经损伤诱发神经性疼痛的干预效果。方法:检索万方、中国知网、PubMed、Embase和Web of Science数据库,检索时限从各数据库建库起至2020年4月,收集跑台、游泳、转轮等运动对大鼠、小鼠坐骨神经损伤诱发疼痛影响的研究。由2位研究者按照纳入标准独立完成文献筛选、资料提取及SYRCLE动物实验偏倚风险评估工具进行方法学质量评价,运用RevMan 5.3和STATA 12.0分析软件进行统计分析。结果:共纳入12篇对照动物实验文献,运动组133只鼠,对照安静组135只鼠。Meta分析结果显示,运动能够显著提高大鼠、小鼠坐骨神经损伤后的机械痛阈值(SMD=0.84,95%CI:0.28-1.40,P=0.003);热痛阈值(SMD=1.54,95%CI:0.93-2.15,P<0.00001)。对坐骨神经损伤后的运动干预时长进行亚组分析,异质性显著降低,术后运动≤3周能显著提高机械痛阈值(SMD=1.04,95%CI:0.62-1.46,P<0.00001);术后运动≤4周能显著提高热痛阈值(SMD=1.93,95%CI:1.19-2.67,P<0.00001)。结论:运动能有效改善大鼠、小鼠坐骨神经损伤产生的机械痛敏和热痛敏。疼痛模型、运动开始时间、运动方式和种属不是影响运动改善疼痛效果的主要因素,而疼痛模型的痛觉敏化时长对运动镇痛效果有重要影响。展开更多
基金supported by the Youth Science and Technology Innovation Special Foundation of Xinjiang Production and Construction Corps, China, No. 2010JC33
文摘The γ-aminobutyric acid neurotransmitter in the spinal cord dorsal horn plays an important role in pain modulation through primary afferent-mediated presynaptic inhibition. The weakening of γ-aminobutyric acid-mediated presynaptic inhibition may be an important cause of neuropathic pain. γ-aminobutyric acid-mediated presynaptic inhibition is related to the current strength of γ-aminobutyric acid A receptor activation. In view of this, the whole-cell patch-clamp technique was used here to record the change in muscimol activated current of dorsal root ganglion neurons in a chronic constriction injury model. Results found that damage in rat dorsal root ganglion neurons following application of muscimol caused concentration-dependent activation of current, and compared with the sham group, its current strength and γ-aminobutyric acid A receptor protein expression decreased. Immunofluorescence revealed that γ-aminobutyric acid type A receptor α2 subunit protein expression decreased and was most obvious at 12 and 15 days after modeling. Our experimental findings confirmed that the y-aminobutyric acid type A receptor α2 subunit in the chronic constriction injury model rat dorsal root ganglion was downregulated, which may be one of the reasons for the reduction of injury in dorsal root ganglion neurons following muscimol-activated currents.
文摘To investigate the neurotoxicity of intrathecal injections of dexmedetomidine,Sprague-Dawley rats were intrathecally injected with dexmedetomidine at doses of 0.75,1.50 and 3.00μg/kg into the spinal dorsal horn.We found that c-Fos expression in the rat spinal dorsal horn peaked at 7 hours following the 3.00μg/kg dexmedetomidine injection,while the levels of c-Fos expression following 0.75 and 1.50μg/kg dexmedetomidine were similar to those in the spinal dorsal horn of normal rats. At 48 hours following administration,the level of c-Fos expression was similar to normal levels.In addition,the intrathecal injections of dexmedetomidine increased paw withdrawal mechanical thresholds and prolonged thermal tail flick latencies.These results indicate that dexmedetomidine has pronounced antinociceptive effects.However,dexmedetomidine appears to have neurotoxic effects in the spinal cord because it increased c-Fos expression in the spinal dorsal horn within 7 hours following administration.
文摘目的:药物治疗神经病理性疼痛的效果有限且不良反应多,而运动是治疗疼痛的一种较好的方式。文章系统性评价运动对大鼠、小鼠坐骨神经损伤诱发神经性疼痛的干预效果。方法:检索万方、中国知网、PubMed、Embase和Web of Science数据库,检索时限从各数据库建库起至2020年4月,收集跑台、游泳、转轮等运动对大鼠、小鼠坐骨神经损伤诱发疼痛影响的研究。由2位研究者按照纳入标准独立完成文献筛选、资料提取及SYRCLE动物实验偏倚风险评估工具进行方法学质量评价,运用RevMan 5.3和STATA 12.0分析软件进行统计分析。结果:共纳入12篇对照动物实验文献,运动组133只鼠,对照安静组135只鼠。Meta分析结果显示,运动能够显著提高大鼠、小鼠坐骨神经损伤后的机械痛阈值(SMD=0.84,95%CI:0.28-1.40,P=0.003);热痛阈值(SMD=1.54,95%CI:0.93-2.15,P<0.00001)。对坐骨神经损伤后的运动干预时长进行亚组分析,异质性显著降低,术后运动≤3周能显著提高机械痛阈值(SMD=1.04,95%CI:0.62-1.46,P<0.00001);术后运动≤4周能显著提高热痛阈值(SMD=1.93,95%CI:1.19-2.67,P<0.00001)。结论:运动能有效改善大鼠、小鼠坐骨神经损伤产生的机械痛敏和热痛敏。疼痛模型、运动开始时间、运动方式和种属不是影响运动改善疼痛效果的主要因素,而疼痛模型的痛觉敏化时长对运动镇痛效果有重要影响。
