CENTRAL NEURAL MEDIATORS OF SECONDARY HYPERALGESIA FOLLOWING HEAT INJURY IN RATS - NEUROPEPTIDES AND EXCITATORY AMINO-ACIDS
CENTRAL NEURAL MEDIATORS OF SECONDARY HYPERALGESIA FOLLOWING HEAT INJURY IN RATS - NEUROPEPTIDES AND EXCITATORY AMINO-ACIDS
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DOI：
10.1016/0304-3940(91)90339-u
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发表时间：
1991-09-30
影响因子：
2.5
通讯作者：
MELZACK, R
中科院分区：
文献类型：
--
作者：
CODERRE, TJ;MELZACK, R
通过检查鞘内（i. t.）在对侧后爪的热损伤之前和之后，在足撤回的膝关节（从48 ℃的水中）上施用受体选择性激动剂和拮抗剂。 在热损伤对侧的后爪中发展的痛觉过敏可以在i. t.注射P物质、神经激肽A和N-甲基-D-天冬氨酸（NMDA），但不注射降钙素基因相关肽（CGRP）、神经激肽B、红藻氨酸或（R，S）-α-氨基-3-羟基-5-甲基异唑-4-丙酸氢溴酸盐（AMPA）。 P物质拮抗剂Arg 1、D-Pro 2、D-Phe 2-D-His 9-substance P和NMDA受体拮抗剂D-2-amino-5-phosphonovalerate（APV）可逆转外侧痛觉过敏，但非NMDA EAA拮抗剂6-cyano-7-nitroquinoxaline-2，3-dione（CNQX）不能逆转外侧痛觉过敏。 当受伤后爪的肢体用C-纤维神经毒素辣椒素预处理时，对侧后爪的痛觉过敏不受影响。 此外，在损伤之前，辣椒素预处理本身在对侧后爪中产生痛觉过敏。 这些结果支持了C-纤维神经肽和EAA对热损伤后中枢神经系统可塑性和继发性痛觉过敏的贡献。
The contribution of C-fiber neuropeptides and excitatory amino acids (EAAs) as central mediators of secondary hyperalgesia was assessed by examining the effects of intrathecal (i.t.) administration of receptor-selective agonists and antagonists on foot-withdrawal latencies (from 48-degrees-C water), both before and after heat injury of the contralateral hindpaw. The hyperalgesia which develops in the hindpaw contralateral to a heat injury, could be reproduced in uninjured rats following i.t. injection of substance P, neurokinin A and N-methyl-D-aspartate (NMDA) but not following calcitonin gene related peptide (CGRP), neurokinin B, kainate or (R,S)-alpha-amino-3-hydroxy-5-methylisozazole-4-propionic acid hydrobromide (AMPA). Contralateral hyperalgesia was reversed by the substance P antagonist Arg1,D-Pro2,D-Phe2-D-His9-substance P, and the NMDA receptor antagonist D-2-amino-5-phosphonovalerate (APV), but not by the non-NMDA EAA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). When the limb of the injured hindpaw was pretreated with the C-fiber neurotoxin capsaicin, hyperalgesia in the contralateral hindpaw was unaffected. Furthermore, prior to injury, the capsaicin pretreatment itself produced hyperalgesia in the contralateral hindpaw. The results give support for a contribution of both C-fiber neuropeptides and EAAs to central nervous system plasticity and secondary hyperalgesia following heat injury.