Wynn Gregory, Ma Bei, Ruan Huai Zhen, Burnstock Geoffrey
Autonomic Neuroscience Institute, Royal Free and University College School of Medicine, London NW3 2PF, United Kingdom.
Am J Physiol Gastrointest Liver Physiol. 2004 Sep;287(3):G647-57. doi: 10.1152/ajpgi.00020.2004.
ATP contributes to mechanosensory transduction in the rat colorectum. P2X3 receptors are present on dorsal root ganglia (DRG) neurons that supply this area of the gut. Previous studies have shown an increased role for ATP in inflamed tissues. We aimed to investigate whether an increased purinergic component exists during mechanosensory transduction in a rat model of colitis. An in vitro rat colorectal preparation was used to investigate whether distension increased ATP release and to evaluate the role of purinergic antagonists in distension-evoked sensory discharges in the pelvic nerve in normal and colitis preparations. DRG neuron purinoceptors were also studied. Distension-evoked responses in the colitis model were attenuated to a significantly greater extent by 2',3'-O-trinitrophenyl-ATP and pyridoxyl 5-phosphate 6-azophenyl-2',4'-disulfonic acid. Inflammation caused augmented distension-evoked sensory nerve excitation after application of ATP and alpha,beta-methylene ATP. Single-fiber analysis confirmed that mean firing per unit was increased. Distension-evoked increases in ATP release from epithelial cells were substantially higher. The number of DRG neurons responding to ATP and the number of those staining for the P2X3 receptor, particularly those containing calcitonin gene-related peptide, were increased. Adenosine, after ectoenzymatic breakdown of ATP, is involved to a lesser degree in the longer-lasting distension-evoked sensory discharge, suggesting reduced ATPase activity. It was therefore concluded that ATP has an enhanced role in mechanosensory transduction in the inflamed rat colorectum. The underlying mechanisms appear to involve increased distension-evoked release of ATP as well as an increase in the number of DRG neurons supplying the colorectum expressing P2X3 receptors, especially those containing calcitonin gene-related peptide.
三磷酸腺苷(ATP)参与大鼠结肠直肠的机械感觉转导。P2X3受体存在于支配肠道该区域的背根神经节(DRG)神经元上。先前的研究表明,ATP在炎症组织中的作用增强。我们旨在研究在大鼠结肠炎模型的机械感觉转导过程中,嘌呤能成分是否增加。使用体外大鼠结肠直肠标本,研究扩张是否会增加ATP释放,并评估嘌呤能拮抗剂在正常和结肠炎标本中扩张诱发的盆神经感觉放电中的作用。还研究了DRG神经元嘌呤受体。在结肠炎模型中,2',3'-O-三硝基苯基-ATP和磷酸吡哆醛6-偶氮苯基-2',4'-二磺酸对扩张诱发反应的抑制作用明显更强。炎症导致在应用ATP和α,β-亚甲基ATP后,扩张诱发的感觉神经兴奋增强。单纤维分析证实单位平均放电增加。上皮细胞扩张诱发的ATP释放增加幅度更大。对ATP有反应的DRG神经元数量以及对P2X3受体染色的神经元数量增加,尤其是那些含有降钙素基因相关肽的神经元。ATP经外切酶分解后产生的腺苷,在持续时间较长的扩张诱发感觉放电中作用较小,提示ATP酶活性降低。因此得出结论,ATP在炎症大鼠结肠直肠的机械感觉转导中作用增强。其潜在机制似乎涉及扩张诱发的ATP释放增加,以及供应结肠直肠的表达P2X3受体的DRG神经元数量增加,尤其是那些含有降钙素基因相关肽的神经元。