Autonomic nerve changes in the mouse pancreas after pancreatic duct ligation.
BACKGROUND
The mouse pancreas exhibits distinct atrophy of the exocrine tissue following pancreatic duct ligation.


OBJECTIVE
To investigate changes of innervation in the whole pancreas after pancreatic duct ligation.


METHODS
The mouse pancreatic duct was ligated at 6 weeks of age. Pancreatic tissues were removed 7 days and 14 days after the ligation, fixed by perfusion and immersion with Zamboni solution, and embedded in gelatin. The whole organ was serially sectioned at a thickness of 100 microm, histochemically stained for cholinesterase, and observed by light microscopy. The number and volume of intrapancreatic ganglia, number of ganglion cells, and volume of each ganglion cell in the whole pancreas were quantitated. Some sections were analyzed using transmission electron microscopy after histochemically staining for cholinesterase.


RESULTS
In the normal pancreas, ganglia were often situated on the outer surface of the islets of Langerhans. Thick nerve bundles ran along the arteries and emanated thin nerve fibers that surrounded the arterioles. In the atrophied pancreas following pancreatic duct ligation, ganglia remained on the islets of Langerhans as in normal mice, while the nerve fibers appeared dense, bending and curling in a more complex manner. The thin nerves also crossed each other in a complex network. Using morphometry in the pancreas following pancreatic duct ligation, the total ganglion cell number was found to decrease from normal levels. The mean ganglion cell volume in the ligated pancreas was significantly smaller than that in normal mice. As observed by transmission electron microscopy, some ganglion cells in the ligated pancreas were negative for cholinesterase activity but were surrounded by positive staining around the surface.


CONCLUSIONS
These results suggest that the function of pancreatic ganglion cells changes with organ atrophy after pancreatic duct ligation.
Okamura
Keisuke
K
Department of Surgical Oncology, Division of Cancer Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido Japan. keisukeo@qb4.so-net.ne.jp
Watanabe
Satoshi
S
Abe
Kazuhiro
K
Kondo
Satoshi
S
Katoh
Hiroyuki
H
D000818:Animals; D001284:Atrophy / Q000209:etiology / Q000473:pathology; D017776:Autonomic Pathways / Q000166:cytology / Q000201:enzymology / Q000502:physiology* / Q000648:ultrastructure; D002802:Cholinesterases / Q000378:metabolism; D005260:Female; D005724:Ganglia / Q000166:cytology / Q000473:pathology / Q000648:ultrastructure; D007150:Immunohistochemistry; D008026:Ligation; D051379:Mice; D010183:Pancreatic Ducts / Q000294:innervation* / Q000473:pathology / Q000601:surgery* / Q000648:ultrastructure
D002802:Cholinesterases