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痛觉调制

痛觉调制的相关文献在1987年到2022年内共计73篇,主要集中在基础医学、中国医学、神经病学与精神病学 等领域,其中期刊论文69篇、会议论文4篇、专利文献38296篇;相关期刊39种,包括石河子大学学报(自然科学版)、中国学术期刊文摘、针刺研究等; 相关会议4种,包括第十二次全国行为医学学术会议、第九届全国针刺麻醉针刺镇痛及针刺调整效应学术研讨会、第九届全国中药药理学术交流会等;痛觉调制的相关文献由154位作者贡献,包括刘文彦、白波、唐敬师等。

痛觉调制—发文量

期刊论文>

论文:69 占比:0.18%

会议论文>

论文:4 占比:0.01%

专利文献>

论文:38296 占比:99.81%

总计:38369篇

痛觉调制—发文趋势图

痛觉调制

-研究学者

  • 刘文彦
  • 白波
  • 唐敬师
  • 刘玉红
  • 吴根诚
  • 宋朝佑
  • 徐满英
  • 李宁
  • 刘海青
  • 印其章
  • 期刊论文
  • 会议论文
  • 专利文献

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    • 刘风雨(译); Aby F; Lorenzo LE; Grivet Z
    • 摘要: 急性痛对机体具有保护作用。过度疼痛激活内源性镇痛系统,从而有效控制疼痛。内源性痛觉调制系统如何参与神经病理性疼痛,近年来备受关注。法国波尔多大学的研究者发现:神经损伤引起脊髓背角氯离子失衡,导致内源性5-HT系统由下行抑制转变为下行易化,进而诱导神经病理性疼痛。第一部分研究主要在正常小鼠上进行,发现RMg的5-HT能神经元投射到脊髓背角,产生内源性镇痛作用(既发挥下行抑制的作用)。
    • 赵舒煊; 张东亮; 沈伟; 冯晓飞; 刘正; 袁文华; 周海宇
    • 摘要: 神经肽Y受体系统是由神经肽Y(NPY)及其哺乳动物体内特异性受体组成的受体-配体系统,广泛参与哺乳动物内痛觉调制,以Y1受体(Y1R)和Y2受体(Y2R)两类亚型为代表.此类受体属G蛋白偶联受体,参与神经元膜信号转导,在中枢神经系统痛觉相关区域广泛分布,不同受体在颅内和脊髓水平分布具有特异性.NPY通过与Y1R和Y2R结合,维持痛觉传递过程的稳态.其中,脊髓水平结合Y1R可发挥镇痛效用,结合Y2R通常可发挥促痛作用.颅内调制功能则与特定区域核团功能有关.
    • 杨坦
    • 摘要: 目的:观察NMDA受体拮抗剂MK801中枢应用对外周电刺激坐骨神经诱导海马CA1区LTP及NR2B表达的影响,探讨电刺激坐骨神经诱导的海马长时程增强的机制.方法:45只雄性SD大鼠随机分为单刺激组、强直刺激组、MK801组,单刺激坐骨神经在海马CA1区诱发场电位,30 min后,单刺激组和强直刺激组侧脑室各注射人工脑脊液(5 μl),MK801组侧脑室注射MK801(500 ng/5μ1),强直刺激组和MK801组给予强直刺激,然后持续给予单刺激2小时,单刺激组一直给予单刺激,观察各组场电位的幅度、潜伏期变化.记录结束后,Western blot的方法检测海马CA1区NR2B的表达.结果:电刺激坐骨神经诱发的海马CA1区LTP被NMDA受体非竞争性受体拮抗剂MK801所抑制.同单刺激组相比,强直刺激组海马NR2B表达升高,而MK801组同单刺激组相比无明显差异.结论:电刺激坐骨神经C类纤维诱导的海马CA1区LTP由NR2B介导.
    • 刘新宇; 苗宇; 杨春晓; 马煦; 王晓坤
    • 摘要: 当今社会日益增长的吗啡等阿片类药物的非法滥用已经严重威胁到人类的健康.然而,迄今为止尚没有找到能够较为有效的防治阿片成瘾的方法.目前研究已知,阿片成瘾的形成所涉及的脑区及核团包括中脑腹侧被盖区(VTA)、伏隔核(NAc)、海马等,其成瘾涉及的神经递质系统包括多巴胺、5-羟色胺等.本文将就多巴胺及海马在痛觉调制及药物成瘾过程中的作用进行综述,为吗啡的成瘾与戒断的进一研究及治疗提供线索.
    • 丰晓溟; 米文丽; 王彦青
    • 摘要: Orexins/Hypocretins是下丘脑生成的兴奋性神经肽,分为OrexinA和OrexinB两种.近年来发现其在痛觉感受和调制中发挥重要角色.Orexin的受体OX1R和OX2R在痛觉下行抑制系统各水平广泛表达是参与痛觉调制的解剖学基础.行为学研究显示,脊髓及脊髓上水平注射Orexins对炎性痛、切口痛、神经痛等模型有不同程度的镇痛效应.中枢神经系统Orexin作用于神经元主要引起兴奋性效应;Orexin作用于中脑导水管灰质腹外侧区神经元突触后膜受体,引起大麻素2-AG释放并逆向传递至突触前膜,通过大麻素受体1抑制γ氨基丁酸(γ-aminobutyric acid,GABA)释放而实现镇痛效应.研究还发现Orexin与强啡肽、内源性大麻素、谷氨酸、GABA等多种神经递质共存也可能是其镇痛效应的物质基础.总之,Orexin可能是一种新的镇痛靶点.
    • 房春燕; 王燕; 王亚南; 孟蒂; 张广学; 李宁
    • 摘要: Objective: To investigate the role of neurite outgrowth inhibitor-A(Nogo-A) and caleitonin gene related peptide 1 (CGRP1) receptor in pain modulation in nucleus aecumbens of rats.Method: Healthy male SD rats were randomly divided into four groups: blank control group (saline was injected to the nucleus aceumbens for 1μl); inflammatory pain model control group (formalin was injected to rat's hindpaw to induce inflammatory pain); morphine group and aloxone group (after inflammatory pain models were prepared, morphine and naloxone were injected to nucleus accumbens for 1μl respectively). The Western blot technique was used for Nogo-A and CGRP1 receptor protein recording. The influence of inflammatory pain, morphine and nalox-one on Nogo-A and CGRP1 receptor protein expression in nucleus accumbens were analyzed.Result: Nogo-A and CGRP1 receptor proteins expressed in nucleus accumbens of normal rats; the expression of Nogo-A protein decreased significantly (P<0.05) and CGRP1 receptor protein increased significantly (P<0.05) afterrnformalin-induced inflammation. Compared with inflammatory pain model control group, the expression of Nogo-A protein increased significantly (P<0.05) and CGRP1 receptor protein decreased significantly (P<0.05) in morphine group; the expression of Nogo-A protein decreased significantly (P<0.05) and CGRP1 receptor protein increased sig- nificantly(P<0.05) in naloxone group.Conclusion: Nogo-A and CGRP were both involved in pain modulation in nucleus accumbens of inflammatory pain rats, and the relationship between Nogo-A and CGRP was negative regulation. Endogenous opioid systems may be influence the role of Nogo-A and CGRP in pain modulation.%目的:探讨大鼠伏核内勿动蛋白A(Nogo-A)和降钙素基因相关肽1(CGRP1)受体在痛觉调制过程中的作用.方法:健康雄性SD大鼠随机分为4组:空白对照组,伏核内注射生理盐水1μl;炎性痛模型对照组、吗啡组和纳洛酮组.福尔马林致炎成功后,分别向其伏核内注射生理盐水、吗啡、纳洛酮各1μl.采用Western blot法,观察各组大鼠伏核内Nogo-A和CGRP1受体蛋白表达的变化,分析炎性痛、吗啡、纳洛酮对大鼠伏核内Nogo-A和CGRP1受体蛋白表达的影响.结果:正常大鼠伏核内有Nogo-A和CGRP1受体蛋白表达;福尔马林致炎后Nogo-A的蛋白表达量降低(P<0.05),而CGRP1表达升高(P<0.05);与炎性痛模型对照组比较,吗啡组大鼠伏核内Nogo-A的蛋白表达量增高(P<0.05),CGRP1降低(P<0.05),而纳洛酮组Nogo-A降低(P<0.05),CGRP1增高(P<0.05).结论:Nogo-A和CGRP参与了炎症致痛敏大鼠伏核内的痛觉调制过程,且二者之间存在反向调节关系,内源性阿片系统可能参与并影响了该过程.
    • 傅小云; 谢鹏; 涂业; 喻田; 吕粟; 龚启勇
    • 摘要: 目的:观察重复伤害性电刺激下大鼠脑功能磁共振成像的变化.方法:健康清洁级SD大鼠24只,麻醉后行4个相同时间段的左前爪重复伤害性电刺激(分别为A、B、C、D,刺激间期为10 min);刺激期间予脑功能磁共振成像扫描,用统计参数法行图像分析不同时间段伤害性电刺激下脑功能成像的变化.结果:不同时间段刺激鼠左前爪激活数目情况:D时间段的总的激活数目显著低于A、B、C时间段,差异有统计学意义(P<0.05);C时间段总的激活数目显著低于A、B时间段,差异有统计学意义(P< 0.05).A、B、C、D时间段伤害性电刺激大鼠均存在明显的局部脑区的血氧水平依赖(blood-oxygenation level-dependent,BOLD)信号的强烈变化,主要激活脑区包括:伏膈核(accumbens nucleus,Acb)、右侧初级感觉皮质(primary somatosensory cortex,SI)、右侧腹后外侧丘脑核(ventral posterolateral thalamic nucleus,VPL)及后扣带回皮质(retrosplenial granular cortex,RSG);在重复伤害性电刺激后,中枢对电刺激引起的躯体感觉传导通路及加工网络的BOLD信号响应减弱.结论:重复伤害性电刺激后,大鼠脑功能成像显示激活脑区数目减少,伏膈核、右侧S1、VPL、RSG脑区激活体素减小,可能与中枢对伤害性刺激的调制有关.
    • 孟蒂; 刘丹; 房春燕; 王燕; 李宁
    • 摘要: Objective: The present study was performed to observe the expression of Nogo-A, substance P (SP) and calcitonin gene-related peptide (CGRP) in periaqueductal gray (PAG) of hyperalgesia rats , and to investigate the role of Nogo-A in pain modulation, and the relationship with CGRP , SP and endogenous opioid system. Methods: 32 male SD rats were randomly divided into four groups: control group received intra-PAG injection of 0.9 % saline (1 μl); Model group, morphine group and naloxone group received unilateral hindpaw hypodermic injection of 1 % formalin (0.1 ml) to prepare pain model, then received intra-PAG injection of 0.9 % saline 1 ul, morphine 1 ul or naloxone 1 μl respectively 3 days later. After 60 minutes , the PAG area of rats were obtained, the expression of Nogo-A, SP and CGRP in PAG of rats in each group were observed and measured by immunohistochemical method. Results: The expression of Nogo-A immunoreactive neuron of model group was obviously reduced than that of control group (P<0.01), but CGRP and SP was obviously increased (P<0.01); The expression of Nogo-A immunoreactive neuron of morphine group was obviously increased than compared with model group(P<0.01), but CGRP and SP was obviously reduced (P < 0.05); The expression of Nogo-A immunoreactive neuron in naloxone group was obviously reduced than that in model group (P<0.05 ), but CGRP and SP was obviously increased (P<0.05). Conclusion: (1) The expression of Nogo-A immunoreactive neuron of model group was obviously reduced than that of control group, but the CGRP and SP were obviously increased . (2) The expression of Nogo-A immunoreactive neuron was obviously increased by opioid system in PAG, but the CGRP and SP were reduced.%目的:用脑内核团微量注射和免疫组化等方法,观察大鼠中脑导水管周围灰质( periaqueductal gray,PAG)内“勿动蛋白”-A(Nogo-A)、P物质(substanceP,SP)和降钙素基因相关肽(calcitoningene-related peptide,CGRP)表达的变化,研究探讨Nogo-A在痛觉调制过程中的角色,以及它在大鼠PAG内与CGRP、SP和内源性阿片系统在痛觉调制过程中的相互作用.方法:选用雄性SD大鼠32只,随机等分为4组:空白对照组8只,分别向PAG内注射0.9%生理盐水1μl;模型对照组、吗啡组和纳洛酮组各8只,首先单侧后爪掌心皮下注射1%的福尔马林0.1 ml复制炎症痛敏大鼠模型,3d后分别向PAG内注射等量0.9%生理盐水、吗啡或纳洛酮各1 μl,60 min后取大鼠大脑PAG区脑组织,采用免疫组化法观测各组大鼠PAG内Nogo-A、SP和CGRP免疫反应阳性神经元的表达差异.结果:与空白对照组比较,模型对照组大鼠PAG内Nogo-A的表达量显著降低(P<0.01),CGRP及SP显著增高(P<0.01);与模型对照组比较,吗啡组大鼠PAG内Nogo-A的表达量显著增高(P<0.01),CGRP及SP显著降低(P<0.05),而纳洛酮组PAG内Nogo-A的表达量显著降低(P<0.05),CGRP及SP显著增高(P<0.05).结论:(1)炎症痛敏大鼠PAG内Nogo-A的表达量比正常降低,而CGRP及SP显著增高;(2)阿片肽可增加PAG内Nogo-A的表达,并降低CGRP及SP的表达.
    • 王燕; 孟蒂; 李宁
    • 摘要: Aim The present study was performed to investigate the role of Nogo-A in pain modulation in the nucleus accumbens ( NAc ) of rats. Methods The inflammatory pain models in rats were prepared in the present study. In different groups,each rat was respectively injected saline , morphine and naloxone to the NAc for 1 μl. After 60 min, the brain tissues in the NAc were obtained. The real time quantitative RT-PCR technique was used for Nogo-A and CGRP mRNA recording and detected the changes of Nogo-A and CGRP mRNA with β-actin as an endogenous control. CT value of Nogo-A and CGRP mRNA in the NAc of rats was recorded and the relative content of every sample against its endogenous control was calculated. The influence of inflammatory pain, morphine or naloxone on Nogo-A and CGRP mRNA expression in the NAc was analyzed. Results Compared with blank control group,the expression of Nogo-A mRNA decreased significantly( P <0. 05 ) and CCRP mRNA increased significantly( P < 0. 01 ) in hyperalgesia model control group. Compared with hyperalgesia model control group ,the expression of Nogo-A mRNA increased significantly( P < 0. 01 ) and CCRP mRNA decreased significantly( P < 0. 05 )in morphine group; and the expression of Nogo-A mRNA decreased significantly( P <0. 05 ) and CGRP mRNA increased significantly( P <0. 05 )in naloxone group. Conclusion When the rats are injected morphine or naloxone to the NAc, the expressions of Nogo-A and CGRP mRNA are both influenced. And the relationship between Nogo-A and CGRP is the negative regulation.%目的 探讨大鼠伏核(nucleus accumbens,NAc)内Nogo-A在痛觉调制过程中的作用.方法 制备炎性痛敏大鼠动物模型,分别向其NAc内注射生理盐水、吗啡或纳洛酮各1 μl,60 min后取大鼠NAc区域脑组织,采用实时定量逆转录聚合酶链式反应 (real-time reverse transcription polymerase chain reaction,RT-PCR) 技术,观察大鼠伏核内Nogo-A mRNA与 CGRP mRNA表达量的改变.实验中以β-actin为内参,记录大鼠伏核内Nogo-A mRNA与CGRP mRNA表达产物的CT值,并计算每一样品对应其内参的相对含量,分析炎性痛、吗啡和纳洛酮对大鼠伏核内Nogo-A mRNA和CGRP mRNA表达的影响.结果 与空白对照组比较,痛敏模型对照组大鼠NAc内Nogo-A mRNA表达量降低(P<0.05),CGRP mRNA增高(P<0.01);与痛敏模型对照组比较,吗啡组Nogo-A mRNA表达量增高(P<0.01),CGRP mRNA降低(P<0.05),而纳洛酮组Nogo-A mRNA表达量降低(P<0.05),CGRP mRNA增高(P<0.05).结论 大鼠NAc注射吗啡和纳洛酮均可影响其Nogo-A 和CGRP mRNA的表达,且Nogo-A与CGRP之间有反向调节关系.
    • 胡玉萍
    • 摘要: Glial cell line-denved neurotrophic factor belongs to the transforming growth factor-b( TCF-b) superfamily, which has many crilical biologic-activity . GDNF is not only a survival factor for midbrain dopaminergic neurons specifically, but has an extensive role in peripheral nervous system and other parts. This article reviewed the role of glial cell line-derived neurotrophic factor and its receptors in nervous system, especially in modulating pain.%胶质细胞源性神经营养因子(glial cell line-derived neurotrophic factor,GDNF)是转化生长因子β(transforming growth fartor-β,TGF-β)超家族成员,具有多种重要的生物学活性,不仅特异性地促进多巴胺能神经元的存活,还对外周神经系统及非神经系统具有广泛的作用.文中就近年来对GDNF及其受体在神经系统中的作用,特别是痛觉调制中作用的国内外研究进展作一综述.
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