Spinal mechanisms underlying persistent pain and referred hyperalgesia in rats with an experimental ureteric stone
Spinal mechanisms underlying persistent pain and referred hyperalgesia in rats with an experimental ureteric stone
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DOI：
10.1152/jn.1998.79.4.1603
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发表时间：
1998-04-01
影响因子：
2.5
通讯作者：
Cervero, F
中科院分区：
文献类型：
--
作者：
Roza, C;Laird, JMA;Cervero, F
大鼠植入实验性输尿管结石后1-4天，脊髓神经元处理来自输尿管的信息，并与正常大鼠进行比较。在结石引起痛觉过敏的情况下，对输尿管进行条件性伤害性刺激的效果也被检测。在脊髓T-12-L-1节段进行细胞外记录。在患有结石的大鼠中，更多的神经元表达输尿管输入(53%比42%)；这样的细胞更有可能表现出背景活动，比正常大鼠更高(6.6%+/-1.2vs.3.2+/-0.9锋/S；平均值+/-SE)，并且随着结石的持续存在而增加。输尿管反应的阈值压力高于正常大鼠(79+/-5对54+/-4毫米汞柱)，但神经元不能编码增加的刺激强度。在患有结石症的大鼠中，35%具有完全无害的躯体感受野的神经元有输尿管输入，而在正常大鼠中没有。对有米输入的神经元施加有害的输尿管扩张，会引起躯体感受器大小和/或躯体输入特性的增加和减少的复杂混合，与对正常动物施加这种刺激时的兴奋性普遍增加明显不同。我们得出结论，输尿管结石的存在引起了脊髓神经元兴奋性的变化(背景活动增强，输尿管驱动细胞数量增加，汇聚的躯体感受野阈值降低)，这可能是结石大鼠出现牵涉痛觉过敏的原因。然而，在存在持续性痛觉过敏的情况下，进一步的伤害性内脏输入会产生选择性变化，这不能用普遍的兴奋性增加来解释，这表明维持痛敏的机制包括中枢抑制系统和兴奋系统的改变。
Spinal neurons processing information from the ureter have been characterized in rats 1-4 days after the implantation of an experimental ureteric stone and compared with those of normal rats. The effects of a conditioning noxious stimulation of the ureter in the presence of the hyperalgesia evoked by the calculosis also were examined. Extracellular recordings were performed at the T-12-L-1 segments of the spinal cord. In rats with calculosis, more neurons expressed a ureter input (53 vs. 42% in normal rats); such cells being more likely to show background activity, at a higher rate than normals (6.6 +/- 1.2 vs. 3.2 +/- 0.9 spikes/s; mean +/- SE) and increasing with the continuing presence of the stone. The threshold pressure for a ureteric response was higher than in normal rats (79 +/- 5 vs. 54 +/- 4 mmHg) but the neurons failed to encode increasing intensities of stimulation. Thirty-five percent of the neurons with exclusively innocuous somatic receptive fields had a ureter input in rats with calculosis, whereas none were seen in normal rats. A noxious ureteric distention applied to neurons with meter input evoked a complex mixture of increases and decreases in somatic receptive held size and/or somatic input properties markedly different from the generalized increases in excitability seen when such a stimulus was applied to normal animals. We conclude that the presence of a ureteric stone evokes excitability changes of spinal neurons (enhanced background activity, greater number of ureter-driven cells, decreased threshold of convergent somatic receptive fields), which likely account for the referred hyperalgesia seen in rats with calculosis. However, further noxious visceral input occurring in the presence of persistent hyperalgesia produces selective changes that cannot be explained by a generalized excitability increase and suggest that the mechanisms underlying maintenance of hyperalgesia include alteration of both central inhibitory and excitatory systems.