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新生大鼠外周炎症后降钙素基因相关肽(CGRP)终末在大鼠背侧的分布模式

The pattern and distribution of calcitonin gene-related peptide (CGRP) terminals in the rat dorsal following neonatal peripheral inflammation.

作者信息

Ling Q D, Chien C C, Wen Y R, Fu W M, Sun W Z

机构信息

Cell Biology and Anatomy Laboratory, Cathay Medical Research Institute, Cathay General Hospital, Taipei.

出版信息

Neuroreport. 2003 Oct 27;14(15):1919-21. doi: 10.1097/00001756-200310270-00007.

Abstract

Neonatal peripheral inflammation has been shown to alter the neural circuitry of the spinal cord in adult rats. However, the temporal and spatial changes in the distribution of primary afferent terminals immediately following a neonatal inflammatory stimulus remains unclear. In the present study we found that intraplantar injection of complete Freund's adjuvant (CFA) or saline alone on postnatal day 1 (P1) causes CGRP immunoreactivity (CGRP-Ir) to gradually increase from P6 to P15 in laminae I and II, and return to baseline at P22. In laminae III and IV, CGRP-Ir markedly increased beginning at P6, and remained elevated thereafter. CGRP-Ir in lamina V remained unchanged throughout the observation period. These findings show that intraplantar CFA induces CGRP-fiber sprouting in laminae III and IV, but not in laminae I, II or V. We suggest that neonatal inflammation causes changes in the neural circuitry pattern in various regions of the dorsal horn during the critical neonatal development period in rats.

摘要

新生儿周围炎症已被证明会改变成年大鼠脊髓的神经回路。然而,新生儿炎症刺激后立即出现的初级传入终末分布的时空变化仍不清楚。在本研究中,我们发现,在出生后第1天(P1)足底内注射完全弗氏佐剂(CFA)或单独注射生理盐水,会使I层和II层中降钙素基因相关肽免疫反应性(CGRP-Ir)从P6到P15逐渐增加,并在P22恢复到基线水平。在III层和IV层,CGRP-Ir从P6开始显著增加,并在之后保持升高。在整个观察期内,V层中的CGRP-Ir保持不变。这些发现表明,足底内注射CFA会诱导III层和IV层中CGRP纤维出芽,但不会诱导I层、II层或V层中CGRP纤维出芽。我们认为,新生儿炎症会在大鼠关键的新生儿发育时期导致背角各区域神经回路模式发生变化。

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