Roza C, Laird J M, Cervero F
Department of Physiology, Faculty of Medicine, University of Alcalá, Alcalá de Henares, E-28871 Madrid, Spain.
J Neurophysiol. 1998 Apr;79(4):1603-12. doi: 10.1152/jn.1998.79.4.1603.
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 T12-L1 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 ureter input evoked a complex mixture of increases and decreases in somatic receptive field 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.
在实验性输尿管结石植入大鼠体内1 - 4天后，对处理来自输尿管信息的脊髓神经元进行了特性分析，并与正常大鼠的相应神经元进行了比较。还研究了在结石病引起的痛觉过敏状态下，对输尿管进行条件性伤害性刺激的影响。在脊髓的T12 - L1节段进行细胞外记录。患有结石病的大鼠中，更多的神经元表现出输尿管输入（53%对正常大鼠的42%）；这类细胞更有可能表现出背景活动，其频率高于正常大鼠（6.6±1.2对3.2±0.9个动作电位/秒；平均值±标准误），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 mmHg），但这些神经元无法编码增强的刺激强度。在患有结石病的大鼠中，35%仅具有无害性躯体感受野的神经元有输尿管输入，而正常大鼠中未观察到此类情况。对有输尿管输入的神经元施加伤害性输尿管扩张，会引起躯体感受野大小和/或躯体输入特性的增加和减少的复杂混合变化，这与对正常动物施加此类刺激时观察到的兴奋性普遍增加明显不同。我们得出结论，输尿管结石的存在会引起脊髓神经元的兴奋性变化（增强的背景活动、更多由输尿管驱动的细胞、会聚性躯体感受野阈值降低），这可能是患有结石病的大鼠出现牵涉性痛觉过敏的原因。然而，在持续痛觉过敏状态下发生的进一步伤害性内脏输入会产生选择性变化，这无法用兴奋性普遍增加来解释，提示痛觉过敏维持的机制包括中枢抑制和兴奋系统的改变。
