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Excessive-ramification and sprouting of intra-pancreatic sensory nerve-fibers in the chronic pancreatitis model.

慢性胰腺炎模型中胰腺内感觉神经纤维的过度分支和出芽。

基本信息

批准号：
16590157
负责人：
YAMADA Hisao
金额：
$ 1.98万
依托单位：
Kansai Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16590157/
关键词：
axonal branching dorsal root ganglia neuronal tracing pain chronic pancreatitis WBN Kob rat immunohistochemistry behavioral study

项目摘要

Increase in number of intrapancreatic nerve bundles has been implicated in the generation of persistent pain in chronic pancreatitis. To examine the origin of these nerve fibers and the mechanisms linking neural morphological change to pain generation, we used neuronal tracing techniques in combination with immunohistochemistry in spontaneous chronic pancreatitis in the WBN/Kob rats.For retrograde tracing, horseradish peroxidase (HRP) was injected into the pancreas, and labeled neurons in the sensory ganglia were counted. For anterograde tracing, biotinylated dextran amine (BDA) was injected into the dorsal root ganglia (DRGs), and labeled intrapancreatic sensory fibers were histochemically assessed. For assessment of pain generation, we evaluated c-Fos-positive neurons in the spinal dorsal horn and behavioral changes of the animals.In WBN/Kob rats, numbers of HRP-labeled neurons were decreased in the DRGs, and numbers of BDA-labeled intrapancreatic nerve fibers and terminals were increased. BDA-labeled nerve fibers contained growth-associated protein-43 (GAP-43). The number of c-Fos-positive neurons in the dorsal horn was also increased and was correlated with intrapancreatic GAP-43-immunoreactivity. Grooming behavior was reduced in WBN/Kob rats and this reduction was facilitated by exocrine stimulation. Axonal branching in DRG neurons innervating the pancreas increases in WBN/Kob rats ; and these morphological changes are likely involved in pain generation in chronic pancreatitis.

胰腺内神经束数量的增加与慢性胰腺炎持续性疼痛的产生有关。为了探讨这些神经纤维的来源以及神经形态改变与疼痛发生之间的联系，我们在WBN/KOB大鼠的自发性慢性胰腺炎模型上采用神经元追踪技术结合免疫组织化学方法，将辣根过氧化物酶(HRP)注入胰腺，并对感觉神经节中标记的神经元进行计数。为了顺行追踪，将生物素化的葡聚糖胺(BDA)注射到背根神经节(DRGs)，并对标记的胰腺内感觉纤维进行组织化学评价。WBN/KOB大鼠脊髓背角c-Fos阳性神经元数量减少，BDA标记的胰腺内神经纤维和终末数量增加。BDA标记的神经纤维含有生长相关蛋白-43(GAP-43)。背角c-Fos阳性神经元数量也增加，并与胰腺内GAP-43免疫反应呈正相关。WBN/KOB大鼠的梳理行为减少，这种减少是由外分泌刺激促进的。在WBN/KOB大鼠中，支配胰腺的DRG神经元的轴突分支增加；这些形态变化可能与慢性胰腺炎疼痛的产生有关。