Responses of rat spinal neurones to natural and electrical stimulation of colonic afferents: effect of inflammation

被引:30
作者
Olivar, T [1 ]
Cervero, F [1 ]
Laird, JMA [1 ]
机构
[1] Univ Alcala de Henares, Dept Physiol, E-28871 Alcala De Henares, Spain
关键词
pain; colon; pelvic nerve; spinal cord; viscera; lamina X;
D O I
10.1016/S0006-8993(00)02274-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Single unit electrical activity has been recorded from 107 neurones excited by electrical stimulation of the pelvic nerve in or around lamina X of the L6-S1 spinal cord in anaesthetised rats. Responses to colorectal distension (CRD; 30 s, 5-80 mmHg) and to somatic electrical and mechanical stimulation were characterised. Of 107 neurones excited by pelvic nerve stimulation, 58 (54%) were affected by CRD: 46 neurones were excited (39 with a sustained response and 7 with an on-off response) and 12 neurones were inhibited. The vast majority of the neurones affected by CRD (54/58) had nociceptive somatic receptive fields. Neurones excited by CRD showed graded stimulus response functions in the noxious range (20-80 mmHg), except for two neurones which only encoded stimulus intensity below 20 mmHg. Neurones inhibited by CRD had significantly larger somatic receptive fields, and more superficial recording sites than those excited by CRD. A group of 12 neurones with sustained excitatory responses to CRD were characterised before and 45 min after intracolonic instillation of 1 ml 0.6% acetic acid. Colon inflammation provoked a significant increase in responses to CRD and to pelvic nerve stimulation (n=12), but no significant change in responses to pinch of their somatic receptive field (n=10). We conclude that of these neurones, the population with excitatory sustained responses to CRD are those likely responsible for processing information leading to acute pain sensations from the colon, and also show central sensitisation after colon inflammation. suggesting they play an important role in development of colonic hyperalgesia. (C) 2000 Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:168 / 177
页数:10
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