Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Lactobacillus species ingestion can decrease autonomic responses and spinal fiber discharge to nociceptive colorectal distension (CRD), even in the absence of inflammation. The present study aimed to determine whether dorsal root ganglion (DRG) somas could be a locus where the antinociceptive probiotic may have an effect. Healthy rats were fed with Lactobacillus reuteri or vehicle control for 9 days whereupon they were anesthetized, and intermittent distal colonic CRD at 80 mmHg distension was either performed for 1 h or not. The animals were immediately euthanized and patch-clamp recordings taken after isolation and overnight culture from those DRG that projected to the distal colon. CRD decreased the threshold for action potential generation and increased the number of spikes discharged during a standard depolarizing test stimulus, and this effect was blocked by prior probiotic ingestion. The increase in excitability was paralleled by an increase in DRG capacitance, which was not altered by Lactobacillus reuteri ingestion. CRD did not increase tissue weight or myeloperoxidase activity. We suggest that the effects of CRD may have been caused by activity-dependent neurotransmission between DRG somas. CRD evoked increases in action potential upstroke speed, which suggests that it may also have led to augmentation of sodium channel conductances. Probiotic ingestion may have interfered with this hypothetical mechanism since it blocked the effect of CRD on the action potential.

摄入乳酸杆菌属物种可降低对伤害性结直肠扩张（CRD）的自主反应和脊髓纤维放电，即使在没有炎症的情况下也是如此。本研究旨在确定背根神经节（DRG）胞体是否可能是抗伤害性益生菌发挥作用的位点。健康大鼠分别喂食罗伊氏乳杆菌或赋形剂对照9天，然后将其麻醉，对80 mmHg扩张压力下的远端结肠进行间歇性CRD操作1小时或不进行操作。立即对动物实施安乐死，并在从投射到远端结肠的那些背根神经节分离并过夜培养后进行膜片钳记录。CRD降低了动作电位产生的阈值，并增加了在标准去极化测试刺激期间发放的峰电位数量，而这种效应可被预先摄入益生菌所阻断。兴奋性的增加与背根神经节电容的增加同时发生，而罗伊氏乳杆菌的摄入并未改变电容。CRD没有增加组织重量或髓过氧化物酶活性。我们认为CRD的效应可能是由背根神经节胞体之间的活动依赖性神经传递引起的。CRD引起动作电位上升速度增加，这表明它可能还导致了钠通道电导的增强。益生菌的摄入可能干扰了这种假设的机制，因为它阻断了CRD对动作电位的影响。