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Using transgenic mouse model of diabetes and controls to examine the histological …


Biology Articles » Biochemistry » Enzymology » Hyperglycemia alters enzyme activity and cell number in spinal sensory ganglia

Abstract
- Hyperglycemia alters enzyme activity and cell number in spinal sensory ganglia

Short report

Hyperglycemia alters enzyme activity and cell number in spinal sensory ganglia

Richard A Zaruba1, Paul N Epstein2 and Patrick A Carr1

1Department of Anatomy and Cell Biology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA
2Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA



Abstract

Peripheral sensory diabetic neuropathy is characterized by morphological, electrophysiological and neurochemical changes to a subpopulation of primary afferent neurons. Here, we utilized a transgenic mouse model of diabetes (OVE26) and age-matched controls to histologically examine the effect of chronic hyperglycemia on the activity or abundance of the enzymes acid phosphatase, cytochrome oxidase and NADPH-diaphorase in primary sensory neuron perikarya and the dorsal horn of the spinal cord. Quantitative densitometric characterization of enzyme reaction product revealed significant differences between diabetic, compared to control, animals for all three enzymes. Levels of acid phosphatase reaction product were found to be significantly reduced in both small diameter primary sensory somata and the dorsal horn. Cytochrome oxidase activity was found to be significantly lower in small primary sensory somata while NADPH-diaphorase labeling was found to be significantly higher in small primary sensory somata and significantly lower in the dorsal horn. In addition to these observed biochemical changes, ratiometric analysis of the number of small versus large diameter primary sensory perikarya in diabetic and control animals demonstrated a quantifiable decrease in the number of small diameter cells in the spinal ganglia of diabetic mice. These results suggest that the OVE26 model of diabetes mellitus produces an identifiable disturbance in specific metabolic pathways of select cells in the sensory nervous system and that this dysfunction may reflect the progression of a demonstrated cell loss.

Journal of Brachial Plexus and Peripheral Nerve Injury 2007, 2:11.  Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).


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