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速激肽拮抗剂和甘丙肽预处理对大鼠坐骨神经切断后脊髓兴奋性过高发展的影响。

The effects of pretreatment with tachykinin antagonists and galanin on the development of spinal cord hyperexcitability following sciatic nerve section in the rat.

作者信息

Luo L, Wiesenfeld-Hallin Z

机构信息

Karolinska Institute, Department of Medical Laboratory Sciences and Technology, Huddinge University Hospital, Sweden.

出版信息

Neuropeptides. 1995 Mar;28(3):161-6. doi: 10.1016/0143-4179(95)90111-6.

DOI:10.1016/0143-4179(95)90111-6
PMID:7540733
Abstract

The effects of acute section of the sciatic nerve on the excitability of the flexor reflex was examined in decerebrate, spinalized, unanaesthetized rats. In control experiments without drugs, the excitability of the flexor reflex was dramatically increased in two phases following axotomy. An early intense, brief reflex hyperexcitability was followed by a less intense, prolonged period of facilitation. The selective NK1 tachykinin receptor antagonist CP-96,345 injected intrathecally at lower (1.2-2.4 nmol) and higher (12 nmol) doses blocked both components of spinal sensitization. The selective NK2 tachykinin receptor antagonist Men 10376 at a dose of 2.4 nmol also reduced both response components, as did the same dose of the inhibitory neuropeptide galanin. Thus, antagonists of excitatory neuropeptides released during and after nerve section, such as substance P and neurokinin A, can block the spinal response to peripheral nerve injury. Furthermore, the inhibitory neuropeptide galanin also reduced spinal cord sensitization.

摘要

在去大脑、脊髓横断、未麻醉的大鼠中,研究了坐骨神经急性切断对屈肌反射兴奋性的影响。在无药物的对照实验中,轴突切断后,屈肌反射的兴奋性在两个阶段显著增加。先是早期强烈、短暂的反射性兴奋性增高,随后是强度较低、持续时间较长的易化期。鞘内注射较低剂量(1.2 - 2.4 nmol)和较高剂量(12 nmol)的选择性NK1速激肽受体拮抗剂CP - 96,345可阻断脊髓敏化的两个成分。剂量为2.4 nmol的选择性NK2速激肽受体拮抗剂Men 10376以及相同剂量的抑制性神经肽甘丙肽也能降低两个反应成分。因此,在神经切断期间及之后释放的兴奋性神经肽(如P物质和神经激肽A)的拮抗剂可阻断脊髓对外周神经损伤的反应。此外,抑制性神经肽甘丙肽也能降低脊髓敏化。

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The effects of pretreatment with tachykinin antagonists and galanin on the development of spinal cord hyperexcitability following sciatic nerve section in the rat.速激肽拮抗剂和甘丙肽预处理对大鼠坐骨神经切断后脊髓兴奋性过高发展的影响。
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