Ritter R C, Ritter S, Ewart W R, Wingate D L
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164.
Am J Physiol. 1989 Nov;257(5 Pt 2):R1162-8. doi: 10.1152/ajpregu.1989.257.5.R1162.
Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.
辣椒素是一种神经毒素，它会破坏具有无髓轴突的小型感觉神经元，包括迷走神经感觉神经元的一个亚群。辣椒素处理可减弱由全身注射胆囊收缩素（CCK）诱导的食物摄入抑制，但对胃扩张诱导的食物摄入抑制无此作用。然而，胃扩张和血管内注射CCK均可通过迷走神经机制改变背侧后脑神经元的放电。因此，一些后脑神经元可能同时接受来自对CCK有反应的辣椒素敏感迷走神经神经元以及对胃扩张有反应的辣椒素不敏感神经元的汇聚输入，这是合理的。为了研究这种可能性，我们在麻醉的完整大鼠和经辣椒素预处理的大鼠动脉内注射八肽胆囊收缩素（CCK-8）期间，对胃扩张反应性后脑神经元进行了细胞外记录。我们发现，经辣椒素预处理的大鼠对CCK-8的神经元放电反应减弱，但对胃扩张的反应未减弱。这些结果与后脑神经元存在对CCK敏感和对胃扩张敏感的汇聚传入输入一致，并表明各种胃肠道感觉模式可能通过对神经毒素敏感性不同的神经元群体传递到大脑。
