Toluene diisocyanate (TDI) induces respiratory allergy in mammals. Using immunohistochemistry and in situ hybridization histochemistry, the present study examined effects of nasal mucosa sensitization by TDI on the immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) and on the expression of their mRNAs in guinea pig trigeminal ganglion and their terminals. Single intranasal application of TDI (acute experiment) did not induce nasal allergy-like behaviours and failed to cause changes of SP and CGRP immunoreactivity and in the expression of preprotachykinin A (PPTA) mRNA and preproCGRP mRNA coding for SP and CGRP respectively in the trigeminal ganglion neurons. However, repeated application of TDI (chronic experiment) caused a dramatic increase of SP and CGRP immunoreactivity in peripheral neurites of sensory nerves in the nasal mucosa but a slight increase in the spinal trigeminal nucleus, a decrease of the same immunoreactivities in the cell bodies of the trigeminal ganglion neurons, and an increase of the expression of PPTA and preproCGRP mRNA in the same neurons. These findings suggest that chronic exposure of the nasal mucosa to TDI apparently causes enhancement of both the biosynthesis of SP and CGRP and their axonal transport in the trigeminal system.

译文

甲苯二异氰酸酯 (TDI) 诱发哺乳动物的呼吸道过敏。本研究使用免疫组织化学和原位杂交组织化学方法,研究了TDI对p物质 (SP) 和降钙素基因相关肽 (CGRP) 的免疫反应性及其在豚鼠三叉神经节及其末端的mrna表达的影响。TDI (急性实验) 的单次鼻内应用不会引起鼻过敏样行为,并且未能引起SP和CGRP免疫反应性的变化以及三叉神经节神经元中分别编码SP和CGRP的protachykinin A (PPTA) mRNA和preproCGRP mRNA的表达。然而,反复应用TDI (慢性实验) 导致鼻粘膜感觉神经末梢神经突中SP和CGRP免疫反应性急剧增加,但脊髓三叉神经核略有增加,三叉神经节神经元细胞体中相同的免疫反应性降低,在相同的神经元中,PPTA和preproCGRP mRNA的表达增加。这些发现表明,鼻粘膜长期暴露于TDI显然会导致SP和CGRP的生物合成及其在三叉神经系统中的轴突转运的增强。

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