Donnerer J, Schuligoi R, Stein C
Department of Experimental and Clinical Pharmacology, University of Graz, Austria.
Neuroscience. 1992 Aug;49(3):693-8. doi: 10.1016/0306-4522(92)90237-v.
The responses of sensory neuropeptides during unilateral, Freund's adjuvant-induced, paw inflammation in the rat were examined. After five days of inflammation, the substance P and calcitonin gene-related peptide content in the sciatic nerve supplying the inflamed paw were increased by 60-75% when compared with the contralateral side. At this time-point, there was also a 30-40% increase in the substance P and calcitonin gene-related peptide content of the dorsal root ganglia (L4-L6), and a 40% increase in the calcitonin gene-related peptide content of the L4-L6 segments of the dorsal spinal cord on the inflammation side. In the dorsal root ganglia, calcitonin gene-related peptide content was also increased as early as 12 h and 48 h after induction of paw inflammation. On day 5 of inflammation, the axonal transport of both sensory neuropeptides towards the inflamed paw, as determined after sciatic nerve ligation, was also markedly increased as compared with the control side. Despite this increased transport, the amount of substance P and calcitonin gene-related peptide present in the inflamed paw itself was either reduced or remained unchanged from day 1 through to day 5 of inflammation pointing towards reduced storage and increased release of the peptides in the inflamed tissue. Nerve growth factor content was markedly increased in the sciatic nerve of the inflamed paw with a peak of +136% at time-point 24 h after induction of inflammation. When rats were systemically treated with anti-nerve growth factor serum, the increase in neuropeptide content in the sciatic nerve of the inflamed paw (day 5) was prevented. On the other hand, local injections of nerve growth factor for 5 days into a noninflamed paw were able to induce an increase in substance P and calcitonin gene-related peptide content in the supplying sciatic nerve. These findings point towards a regulatory function for nerve growth factor in vivo in the stimulation of sensory neuropeptide synthesis during prolonged inflammatory processes.
研究了大鼠单侧弗氏佐剂诱导的爪部炎症过程中感觉神经肽的反应。炎症五天后,与对侧相比,供应发炎爪部的坐骨神经中P物质和降钙素基因相关肽含量增加了60 - 75%。此时,背根神经节(L4 - L6)中P物质和降钙素基因相关肽含量也增加了30 - 40%,炎症侧脊髓背段L4 - L6节段的降钙素基因相关肽含量增加了40%。在背根神经节中,早在爪部炎症诱导后12小时和48小时,降钙素基因相关肽含量就已增加。在炎症第5天,坐骨神经结扎后测定,两种感觉神经肽向发炎爪部的轴突运输与对照侧相比也显著增加。尽管运输增加,但从炎症第1天到第5天,发炎爪部自身的P物质和降钙素基因相关肽含量要么减少,要么保持不变,这表明发炎组织中肽的储存减少而释放增加。发炎爪部坐骨神经中的神经生长因子含量显著增加,在炎症诱导后24小时时间点达到峰值+136%。当给大鼠全身注射抗神经生长因子血清时,发炎爪部坐骨神经(第5天)中神经肽含量的增加被阻止。另一方面,向未发炎的爪部局部注射神经生长因子5天,能够诱导供应该爪部的坐骨神经中P物质和降钙素基因相关肽含量增加。这些发现表明神经生长因子在体内对长期炎症过程中感觉神经肽合成的刺激具有调节作用。