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首页> 外文期刊>Cell and Tissue Research >Sustained neurochemical plasticity in central terminals of mouse DRG neurons following colitis.
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Sustained neurochemical plasticity in central terminals of mouse DRG neurons following colitis.

机译:结肠炎后,小鼠DRG神经元中央末端的神经化学可塑性持续保持。

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摘要

Sensitization of dorsal root ganglia (DRG) neurons is an important mechanism underlying the expression of chronic abdominal pain caused by intestinal inflammation. Most studies have focused on changes in the peripheral terminals of DRG neurons in the inflamed intestine but recent evidence suggests that the sprouting of central nerve terminals in the dorsal horn is also important. Therefore, we examine the time course and reversibility of changes in the distribution of immunoreactivity for substance P (SP), a marker of the central terminals of DRG neurons, in the spinal cord during and following dextran sulphate sodium (DSS)-induced colitis in mice. Acute and chronic treatment with DSS significantly increased SP immunoreactivity in thoracic and lumbosacral spinal cord segments. This increase developed over several weeks and was evident in both the superficial laminae of the dorsal horn and in lamina X. These increases persisted for 5 weeks following cessation of both the acute and chronic models. The increase in SP immunoreactivity was not observed in segments of the cervical spinal cord, which were not innervated by the axons of colonic afferent neurons. DRG neurons dissociated following acute DSS-colitis exhibited increased neurite sprouting compared with neurons dissociated from control mice. These data suggest significant colitis-induced enhancements in neuropeptide expression in DRG neuron central terminals. Such neurotransmitter plasticity persists beyond the period of active inflammation and might contribute to a sustained increase in nociceptive signaling following the resolution of inflammation.
机译:背根神经节(DRG)神经元的敏化是表达肠道炎症引起的慢性腹痛的重要机制。大多数研究集中在发炎的肠道中DRG神经元末梢的变化,但最近的证据表明,背角中枢神经末梢的萌发也很重要。因此,我们研究了葡聚糖硫酸钠(DSS)诱发的结肠炎期间和之后,脊髓中DRG神经元中央末端的标记物P(SP)的免疫反应性分布的时程和可逆性。老鼠。 DSS的急性和慢性治疗可显着增加胸部和腰s部脊髓节段的SP免疫反应性。这种增加持续了数周,并且在背角的浅层和X椎板均可见。这些增加在急性和慢性模型停止后持续了5周。在颈脊髓节段中未观察到SP免疫反应性的增加,这些节段不受结肠传入神经元轴突的支配。急性DSS结肠炎后解离的DRG神经元与对照小鼠解离的神经元相比,神经突发芽增加。这些数据表明结肠炎引起的DRG神经元中央终端神经肽表达的明显增强。这种神经递质可塑性在活动性炎症期之后仍持续存在,并且可能有助于炎症消退后伤害感受信号的持续增加。

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