help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schmidt, R. E.
Right arrow Articles by Johnson, E. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schmidt, R. E.
Right arrow Articles by Johnson, E. M., Jr

American Journal of Pathology, Vol 103, 210-225, Copyright © 1981 by American Society for Investigative Pathology

REGULAR ARTICLES

Experimental diabetic autonomic neuropathy

RE Schmidt, JS Nelson and EM Johnson Jr

The regular occurrence of autonomic neuropathy, colonic dilatation, and loss of fecal consistency was investigated in streptozotocin-diabetic, age-matched control, and pancreatic-islet--transplanted rats using ultrastructural, histochemical, and biochemical methods. Degenerating unmyelinated axons were observed by electron microscopy in the colonic submucosa and muscularis, ileal mesentery, and splenic pedicle in 5--7 months diabetic animals; similar changes were not found in control rats or animals subjected to islet transplantation three weeks after induction of diabetes and sacrificed 4--6 months later (colon only). Regenerative changes, including axons with identifiable growth cones, were demonstrated in the mesenteric nerves of chronically diabetic animals. Formaldehyde-induced catecholamine fluorescence and cholinesterase histochemistry suggested deficiencies in colonic adrenergic and cholinergic innervation; histochemical findings in islet- transplanted animals were comparable to those of untreated control animals. Biochemical measurements of the adrenergic and cholinergic nervous system marker enzymes dopamine-beta-hydroxylase and choline acetyltransferase, respectively, in colon and spleen confirm a deficit in adrenergic (colon and spleen) and cholinergic (colon) innervation in chronically diabetic animals.


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
R. E. Schmidt, D. A. Dorsey, L. N. Beaudet, K. E. Frederick, C. A. Parvin, S. B. Plurad, and M. G. Levisetti
Non-Obese Diabetic Mice Rapidly Develop Dramatic Sympathetic Neuritic Dystrophy: A New Experimental Model of Diabetic Autonomic Neuropathy
Am. J. Pathol., November 1, 2003; 163(5): 2077 - 2091.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
R. E. Schmidt, D. A. Dorsey, L. N. Beaudet, S. B. Plurad, C. A. Parvin, and M. S. Miller
Insulin-like Growth Factor I Reverses Experimental Diabetic Autonomic Neuropathy
Am. J. Pathol., November 1, 1999; 155(5): 1651 - 1660.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1981 by the American Society for Investigative Pathology.