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本文首先用免疫组化链霉卵白素-生物素（LSAB）技术观察到，在大鼠右踝外侧皮下注射弗氏完全佐剂，引起急性关节炎和继发的多发性关节炎时，可分别使注射同侧和双侧L5背根节中CGRP－IR阳性细胞数明显增多。进一步用核酸分子原位杂交技术观察了大鼠背根节中α－CGRP和β-CGRPmRNAs的表达。在注射性剂后第2d，背根节中标记α－CGRP和β－CGRP的细胞数增多，银粒密度增加；在注射佐剂后第15d形成多发性关节炎时两者进一步增加，主要是被标记的小细胞数增多（分别为28．48％和30．29％），标记细胞的银粒密度也进一步增加。以上结果说明，佐剂性关节炎刺激可使正常情况下不合成（或合成量很少）CGRP的初级传入神经元，明显地上调CGRP的合成。上述免疫组化和原位杂交实验的结果与佐剂性关节炎的发展相平行，提示在背根节中CGRP的变化与性剂性关节炎的发生、发展密切相关。
In this paper, we first observed by immunohistochemical streptavidin-biotin (LSAB) technique that when subcutaneous injection of complete Freund’s adjuvant in the right lateral malleolus of rats caused acute arthritis and secondary polyarthritis, The number of CGRP-IR positive cells in the ipsilateral and bilateral L5 dorsal root ganglia was significantly increased. The expression of α-CGRP and β-CGRP mRNA in rat dorsal root ganglia was further observed by in situ hybridization. On the 2nd day after injection of the injectable agent, the number of a-CGRP and β-CGRP-labeled cells in the dorsal root ganglia increased and the density of silver grains increased. Both of them increased further The number of labeled small cells increased (28.48% and 30.29% respectively), and the densities of silver particles in labeled cells increased further. The above results indicate that adjuvant arthritis stimulation can lead to normal primary uninformed (or less synthetic) primary afferent neurons of CGRP and significantly upregulate the synthesis of CGRP. The results of immunohistochemistry and in situ hybridization experiments parallel with the development of adjuvant arthritis suggest that the changes of CGRP in DRG are closely related to the occurrence and development of ASA.