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本文引用的文献

1
Bradykinin evokes a Ca2+-activated chloride current in non-neuronal cells isolated from neonatal rat dorsal root ganglia.缓激肽可在从新生大鼠背根神经节分离出的非神经元细胞中诱发一种钙激活氯离子电流。
J Physiol. 2001 Feb 1;530(Pt 3):395-403. doi: 10.1111/j.1469-7793.2001.0395k.x.
2
Prostaglandin E2-induced sensitization of bradykinin-evoked responses in rat dorsal root ganglion neurons is mediated by cAMP-dependent protein kinase A.前列腺素E2诱导的大鼠背根神经节神经元中缓激肽诱发反应的致敏作用由环磷酸腺苷(cAMP)依赖性蛋白激酶A介导。
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The effects of changing intracellular Ca2+ buffering on the excitability of cultured dorsal root ganglion neurones.改变细胞内钙离子缓冲对培养的背根神经节神经元兴奋性的影响。
Neurosci Lett. 1999 Aug 27;271(3):171-4. doi: 10.1016/s0304-3940(99)00538-8.
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Specific involvement of PKC-epsilon in sensitization of the neuronal response to painful heat.蛋白激酶C-ε在神经元对热痛觉反应敏化中的特异性作用。
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Temperature coefficient of membrane currents induced by noxious heat in sensory neurones in the rat.大鼠感觉神经元中有害热诱导的膜电流的温度系数
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Glutamate-dependent astrocyte modulation of synaptic transmission between cultured hippocampal neurons.谷氨酸依赖的星形胶质细胞对培养海马神经元间突触传递的调节
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Inflammatory mediators at acidic pH activate capsaicin receptors in cultured sensory neurons from newborn rats.酸性pH值下的炎症介质可激活新生大鼠培养感觉神经元中的辣椒素受体。
J Neurophysiol. 1998 Feb;79(2):670-6. doi: 10.1152/jn.1998.79.2.670.
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Heat transduction in rat sensory neurons by calcium-dependent activation of a cation channel.大鼠感觉神经元中阳离子通道钙依赖性激活介导的热传导
Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):7006-11. doi: 10.1073/pnas.94.13.7006.
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An interaction of inflammatory mediators and protons in small diameter dorsal root ganglion neurons of the rat.大鼠小直径背根神经节神经元中炎症介质与质子的相互作用。
Neurosci Lett. 1997 Mar 7;224(1):37-40. doi: 10.1016/s0304-3940(97)13450-4.

缓激肽对新生大鼠背根神经节神经元的间接作用:非神经元细胞作为伤害感受器的作用。

Indirect actions of bradykinin on neonatal rat dorsal root ganglion neurones: a role for non-neuronal cells as nociceptors.

作者信息

Heblich F, England S, Docherty R J

机构信息

Centre for Neuroscience, Sensory Function, Hodgkin Building, King's College London, Guy's Campus, London SE1 1UL, UK.

出版信息

J Physiol. 2001 Oct 1;536(Pt 1):111-21. doi: 10.1111/j.1469-7793.2001.00111.x.

DOI:10.1111/j.1469-7793.2001.00111.x
PMID:11579161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2278851/
Abstract
  1. In this study we have investigated the action of bradykinin (Bk) on cultured neonatal rat dorsal root ganglion (DRG) cells, with the aim of elucidating whether the neuronal response to Bk is influenced by association with non-neuronal satellite cells. 2. Bradykinin (100 nM) evoked an inward current (I(Bk)) in 51 of 58 voltage clamped DRG neurones (holding potential (V(h)) = -80 mV) that were in contact with non-neuronal satellite cells. 3. Bradykinin failed to evoke an inward current in isolated DRG neurones (V(h) = -80 mV) that were not in contact with non-neuronal satellite cells (n = 41). 4. The lack of neuronal response to Bk was not influenced by time in culture. Bradykinin failed to evoke a response in isolated neurones through 1-5 days in culture. By contrast neurones in contact with satellite cells responded to Bk throughout the same time period. 5. Failure of isolated neurones to respond to Bk was not due to the replating procedure or to selective subcellular distribution of receptors/ion channels to the processes rather than the somata of neurones. 6. Using Indo-1 AM microfluorimetry Bk (100 nM) was demonstrated to evoke an intracellular Ca(2+) increase (Ca(Bk)) in DRG neurones in contact with non-neuronal satellite cells and in isolated neurones. 7. These data suggest that the inward current response to Bk requires contact between DRG neurones and non-neuronal satellite cells. This implies an indirect mechanism of action for Bk via the non-neuronal cells, which may perform a nociceptive role. However, Bk can also act directly on the neurones, since it evokes Ca(Bk) in isolated neurones. The relationship between Ca(Bk) and the Bk-induced inward current is unknown at present.
摘要
  1. 在本研究中,我们研究了缓激肽(Bk)对培养的新生大鼠背根神经节(DRG)细胞的作用,目的是阐明神经元对Bk的反应是否受与非神经元卫星细胞结合的影响。2. 缓激肽(100 nM)在58个与非神经元卫星细胞接触的电压钳制DRG神经元中的51个中诱发了内向电流(I(Bk))(钳制电位(V(h))=-80 mV)。3. 缓激肽未能在未与非神经元卫星细胞接触的分离DRG神经元(V(h)=-80 mV)中诱发内向电流(n = 41)。4. 神经元对Bk缺乏反应不受培养时间的影响。在培养1 - 5天期间,缓激肽未能在分离的神经元中诱发反应。相比之下,与卫星细胞接触的神经元在同一时间段内对Bk有反应。5. 分离的神经元对Bk无反应并非由于重新接种过程或受体/离子通道在神经元的突起而非胞体中的选择性亚细胞分布。6. 使用 Indo-1 AM 微量荧光测定法证明,缓激肽(100 nM)可在与非神经元卫星细胞接触的DRG神经元以及分离的神经元中诱发细胞内Ca(2+)增加(Ca(Bk))。7. 这些数据表明,对Bk的内向电流反应需要DRG神经元与非神经元卫星细胞之间的接触。这意味着Bk通过非神经元细胞发挥间接作用机制,非神经元细胞可能发挥伤害感受作用。然而,Bk也可直接作用于神经元,因为它能在分离的神经元中诱发Ca(Bk)。目前尚不清楚Ca(Bk)与Bk诱导的内向电流之间的关系。