Neuronal preservation in the sympathetic ganglia of rats with chronic streptozotocin-induced diabetes.
Recent studies have reported that rat sympathetic neurons exposed to increased concentrations of glucose in vitro initiate an apoptotic program which culminates in neuronal cell death, a process proposed to contribute to the development of human diabetic autonomic neuropathy. We tested this hypothesis in an in vivo streptozotocin model of diabetic autonomic neuropathy using an unbiased counting method to quantitate neuron numbers in control and diabetic rats. Ten months of severe untreated diabetes failed to produce significant neuron loss in either the rat superior mesenteric or superior cervical sympathetic ganglia indicating that apoptotic neuronal cell death is unlikely to play a role in the pathogenesis of experimental diabetic autonomic neuropathy.
Schmidt
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Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. reschmidt@pathology.wustl.edu
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002452:Cell Count; D002470:Cell Survival / Q000502:physiology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D003929:Diabetic Neuropathies / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D005728:Ganglia, Sympathetic / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley