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首页> 外文期刊>The European Journal of Neuroscience >Exogenous NT-3 and NGF differentially modulate PACAP expression in adult sensory neurons, suggesting distinct roles in injury and inflammation.
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Exogenous NT-3 and NGF differentially modulate PACAP expression in adult sensory neurons, suggesting distinct roles in injury and inflammation.

机译：外源NT-3和NGF差异性调节成年感觉神经元中的PACAP表达，提示在损伤和炎症中的不同作用。

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摘要

Expression of pituitary adenylate cyclase-activating polypeptide in sensory neurons varies with injury or inflammation. The neurotrophins NGF and NT-3 are profound regulators of neuronal peptidergic phenotype in intact and injured sensory neurons. This study examined their potential for modulation of PACAP expression in adult rat with intact and injured L4-L6 spinal nerves with or without immediate or delayed intrathecal infusion of NT-3 or NGF. Results indicate that in L5 DRG, few trkC neurons express high levels of PACAP mRNA in the intact state, but many do following injury. The elevated expression in injured neurons is mitigated by NT-3 infusion, suggesting a role for NT-3 in returning the 'injured phenotype' back towards an 'intact phenotype'. NGF dramatically up-regulated PACAP expression in trkA-positive neurons in both intact and injured DRGs, implicating NGF as a positive regulator of PACAP expression in nociceptive neurons. Surprisingly, NT-3 modulates PACAP expression in an antagonistic fashion to NGF in intact neurons, an effect most evident in the trkA neurons not expressing trkC. Both NT-3 and NGF infusion results in decreased detection of PACAP protein in the region of the gracile nuclei, where central axons of the peripherally axotomized large sensory fibers terminate. NGF infusion also greatly increased the amount of PACAP protein detected in the portion of the dorsal horn innervated by small-medium size DRG neurons, while both neurotrophins appear able to prevent the decrease in PACAP expression observed in these afferents with injury. These results provide the first insights into the potential molecules implicated in the complex regulation of PACAP expression in sensory neurons.
机译：垂体腺苷酸环化酶激活多肽在感觉神经元中的表达随损伤或炎症而变化。神经营养蛋白NGF和NT-3是完整和受损感觉神经元中神经元肽能表型的重要调节剂。这项研究检查了它们在成年大鼠L4-L6脊髓神经完整和受损时，无论是否立即或延迟鞘内输注NT-3或NGF均能调节PACAP表达。结果表明，在L5 DRG中，很少有trkC神经元在完整状态下表达高水平的PACAP mRNA，但许多在损伤后确实表达。 NT-3注入可减轻受损神经元的表达升高，表明NT-3在使“损伤表型”返回“完整表型”中发挥作用。 NGF显着上调了完整DRG和受损DRG中trkA阳性神经元中PACAP的表达，暗示NGF作为伤害性神经元中PACAP表达的正调节剂。令人惊讶的是，NT-3以完整神经元中NGF的拮抗方式调节PACAP表达，这种作用在不表达trkC的trkA神经元中最明显。 NT-3和NGF的注入都会导致在细核的区域中PACAP蛋白的检测减少，在该区域中，外围轴突化的大型感觉纤维的中央轴突终止了。 NGF输注还大大增加了在中小尺寸DRG神经元支配的背角部分中检测到的PACAP蛋白的量，而两种神经营养蛋白似乎都能够防止在这些受伤的传入细胞中观察到PACAP表达的下降。这些结果提供了对潜在的分子的初步见解，这些潜在的分子与感觉神经元中PACAP表达的复杂调控有关。

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