Thalamic modulation of visceral nociceptive processing in adult rats with neonatal colon irritation.
Thalamic modulation of visceral nociceptive processing in adult rats with neonatal colon irritation.
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丘脑对新生大鼠结肠刺激内脏伤害性处理的调节。
DOI：
10.1016/j.brainres.2004.01.083
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Al-Chaer,ElieD
中科院分区：
文献类型：
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作者：
Saab,CarlY;Park,YoungC;Al-Chaer,ElieD
内脏痛起源于内脏器官对伤害性刺激的反应，如果持续时间长，可能导致介导内脏伤害性感受的神经网络的慢性变化。例如，结肠炎症增强了丘脑中神经元对结肠直肠扩张（CRD）的反应，而背柱（DC）中的病变逆转了这种神经元敏化，表明丘脑和DC在慢性内脏痛中起主要作用。在这项研究中，我们使用成年大鼠致敏与新生儿疼痛结肠刺激揭示的贡献丘脑和DC的神经元过度兴奋的慢性内脏痛模型。我们记录了对照组大鼠和刺激或失活丘脑后结肠刺激大鼠以及DC损伤后的腰骶神经元对CRD的反应。结果表明：（1）刺激丘脑后，对照组神经元对CRD的反应减弱，而刺激结肠后，反应减弱或增强;（2）DC损伤分别减弱或增强了正调制组和负调制组神经元对CRD的反应;第三，丘脑注射利多卡因可减少结肠刺激大鼠的某些神经元对CRD的反应，但对对照大鼠的反应无影响。因此，可以合理地推测，结肠刺激大鼠的可塑性可能是慢性疼痛的基础，是通过DC中的反馈回路上升和丘脑参与来维持的。
Visceral pain originates from visceral organs in response to a noxious stimulus which, if prolonged, may lead to chronic changes in the neural network mediating visceral nociception. For instance, colon inflammation enhances the responses of neurons in the thalamus to colorectal distension (CRD), whereas lesion in the dorsal column (DC) reverses this neuronal sensitization, suggesting that the thalamus and the DC play major roles in chronic visceral pain. In this study, we used adult rats sensitized with neonatal painful colon irritation to reveal the contribution of the thalamus and the DC to neuronal hyperexcitability in a model of chronic visceral pain. We recorded the responses of lumbosacral neurons to CRD in control rats and in rats with colon irritation following stimulation or inactivation of the thalamus, and after DC lesion. Our results show that, first, neuronal responses to CRD decreased following thalamic stimulation in control rats, whereas, in rats with colon irritation, responses either decreased or increased; second, DC lesion attenuated or enhanced these effects in the positively or in the negatively modulated group of neurons, respectively; third, lidocaine injection in the thalamus reduced the responses to CRD in some of the neurons recorded in rats with colon irritation, but had no effect on those in control rats. Therefore, it is reasonable to speculate that plasticity in rats with colon irritation that may underlie chronic pain is sustained by feedback loops ascending in the DC and engaging the thalamus.