Pantellev S S, Martseva A A, Liubashina O A
Ross Fiziol Zh Im I M Sechenova. 2011 Dec;97(12):1336-45.
In experiments on anaesthetized rats, the neuronal mechanisms underlying processing of the nociceptive information from the colon within the nucleus of the solitary tract were studied. In addition, the role of nitric oxide in these processes was estimated. Analysis of changes in c-fos expression revealed that nociceptive colorectal distension (CRD) resulted in activation of neurons mainly in the medial, commissural, parvicellular and dorsomedial subnuclei of the solitary tract nucleus. Non-noxious CRD evoked in these subdivisions weak phasic excitatory neuronal responses. Under noxious CRD, neurons with phasic (58%) and tonic (42%) responses were revealed. The phasic neuron responses were significantly enhanced in comparison with non-noxious CRD. Inhibition of the neuronal NO-syntheses resulted in significant decrease of neuron responses to noxious CRD and the number of cells with tonic reactions. Therefore, neurons with tonic responses may be directly related to NO-depended processing ofnociceptive information from colon.
在对麻醉大鼠进行的实验中,研究了孤束核内处理来自结肠的伤害性信息的神经元机制。此外,评估了一氧化氮在这些过程中的作用。对c-fos表达变化的分析表明,伤害性结肠扩张(CRD)主要导致孤束核内侧、连合、小细胞和背内侧亚核的神经元激活。在这些亚区中,非伤害性CRD引起微弱的阶段性兴奋性神经元反应。在伤害性CRD作用下,发现了具有阶段性(58%)和持续性(42%)反应的神经元。与非伤害性CRD相比,阶段性神经元反应显著增强。抑制神经元型一氧化氮合酶导致对伤害性CRD的神经元反应以及具有持续性反应的细胞数量显著减少。因此,具有持续性反应的神经元可能与来自结肠的伤害性信息的一氧化氮依赖性处理直接相关。