Abstract
Central projections of vagal motoneurons to the heart were studied in diabetic rats using Wheat germ Agglutinin-Horseradish peroxidase (WGA-HRP). Experimental rats were rendered diabetic by intraperitoneal injection of streptozotocin in citrate buffer. The diabetic rats were maintained in a stable diabetic state by daily injection of insulin for 24 weeks. Age-matched control rats were injected intraperitoneally with citrate buffer not containing streptozotocin. Control rats were also kept alive for 24 weeks after citrate buffer injection. At the end of 24 weeks the two groups were prepared for injection with WGA-HRP. Following anesthesia with sodium pentobarbitone, thoracotomy was performed on the left aspect of the thorax to expose the heart. The atrial and ventricular walls were then injected with 5% WGA-HRP by multiple intramuscular penetrations. Experimental and control rats were sacrificed 72 h after tracer injection by transcardial perfusion first with normal saline followed by fixative and then buffered sucrose. Transverse serial frozen sections of the brainstem were then taken and processed for WGA-HRP neurohistochemistry and analyzed under light and dark-field microscopy. Analysis of the sections taken from diabetic rats revealed fewer WGA-HRP labeled neurons in the nucleus ambiguus (nA) than sections taken from control rats. Sporadic labeling of the dorsal motor nucleus of the vagus nerve was observed in control rat but not in the diabetic rats. It was concluded that the depletion of labeled neurons in the diabetic rats compared with the normoglycaemic rats is indicative of impairment of retrograde neuronal transport of WGAHRP in chronic diabetic state.
Highlights
Diabetic-induced peripheral neuropathy is a significant complication resulting in increased patient morbidity and mortality
Whereas the impairment in the ability of the vagus nerve to transport target tissue-derived endogenous material such as Nerve Growth Factor (NGF) and NT-3 has been demonstrated in the diabetic rat, no change was recorded in the content of these materials in the vagally innervated organs studied[11]
Since a healthy living neuron is actively involved in the transport of materials between the axonal terminals, dendrites and the cell body, it has been hypothesized that neuronal functional abnormalities such as observed in the diabetic state are accompanied by disruptions in the mechanism of neuronal transport in the affected vagus nerve
Summary
Diabetic-induced peripheral neuropathy is a significant complication resulting in increased patient morbidity and mortality. Since a healthy living neuron is actively involved in the transport of materials between the axonal terminals, dendrites and the cell body, it has been hypothesized that neuronal functional abnormalities such as observed in the diabetic state are accompanied by disruptions in the mechanism of neuronal transport in the affected vagus nerve. This hypothesis is supported by the demonstration of impairment of anterograde and retrograde transport of NGF, neurotrophins and the neuronal tracer, Fluorogold in the vagus nerve of STZ-induced chronic diabetic states[5,11]. The paucity of literature on this subject motivated the present study which was designed to determine the effect of STZinduced diabetes on the retrograde transport of a sensitive neuronal tracer, WGA-HRP by cardiac preganglionic parasympathetic vagal nerve fibres in the rat
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
