Effect of streptozotocin-induced diabetes on NGF, P75(NTR) and TrkA content of prevertebral and paravertebral rat sympathetic ganglia

Robert E. Schmidt, Denise A. Dorsey, Kevin A. Roth, Curtis A. Parvin, Luke Hounsom, David R. Tomlinson

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Diabetic autonomic neuropathy results in significant morbidity and mortality. Both diabetic humans and experimental animals show neuroaxonal dystrophy of autonomic nerve terminals, particularly in the prevertebral superior mesenteric ganglia (SMG) and celiac ganglia (CG) which innervate the hyperplastic/hypertrophic diabetic small intestine. Previously, investigators suggested that disturbances in ganglionic nerve growth factor (NGF) content or transport might play a pathogenetic role in diabetic autonomic pathology. To test this hypothesis, we measured NGF content and NGF receptor expression, p75(NTR) (low affinity neurotrophin receptor) and trkA (high affinity NGF receptor), in control and diabetic rat SMG, CG and superior cervical ganglia (SCG). Surprisingly, rather than a decrease, we observed an approximate doubling of NGF content in the diabetic SMG and CG, a result which reflects increased NGF content in the hyperplastic diabetic alimentary tract. No change in NGF content was detected in the diabetic SCG which is relatively spared in experimental diabetic autonomic neuropathy. NGF receptor expression was not consistently altered in any of the autonomic ganglia. These observations suggest that increased NGF content in sympathetic ganglia innervating the diabetic alimentary tract coupled with intact receptor expression may produce aberrant axonal sprouting and neuroaxonal dystrophy. (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)149-156
Number of pages8
JournalBrain Research
Volume867
Issue number1-2
DOIs
StatePublished - Jun 9 2000

Keywords

  • Diabetic autonomic neuropathy
  • Neuroaxonal dystrophy

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