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-cGMP pathway may be functionally relevant in the nodose ganglion and at afferent terminations of the vagus nerve. The technique of unilateral vagal ligations, using double ligatures, was combined with the techniques of NADPH-diaphorase histochemistry, as an index of nitric oxide synthase (NOS) activity, and autoradiography using the radioligands [3H]nitro-
doi:10.1016/S0006-8993(02)02645-8 
Published by Elsevier Science B.V.
Research report
Streptozotocin-induced diabetes reduces retrograde axonal transport in the afferent and efferent vagus nerve*1
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Accepted 19 February 2002.
Abstract
Diabetes-induced alterations in nerve function include reductions in the retrograde axonal transport of neurotrophins. A decreased axonal accumulation of endogenous nerve growth factor (NGF) and neurotrophin-3 (NT-3) in the vagus nerve of streptozotocin (STZ)-induced diabetic rats was previously shown. In the current study, no changes in the NGF and NT-3 protein or mRNA levels in the stomach or atrium, two vagally innervated organs, were noted after 16 or 24 weeks of diabetes. Moreover, the amounts of neurotrophin receptor (p75, TrkA, TrkC) mRNAs in the vagus nerve and vagal afferent nodose ganglion were not reduced in diabetic rats. These data suggest that neither diminished access to target-derived neurotrophins nor the loss of relevant neurotrophin receptors accounts for the diabetes-induced alteration in the retrograde axonal transport of neurotrophins. To assess whether diabetes causes a defect in axonal transport that may not be specific to neurotrophin transport, we studied the ability of a neuronal tracer (FluoroGold, FG) to be retrogradely transported by vagal neurons of control and diabetic rats. After vagal target tissue (stomach) injections of FG, the numbers of FG-labeled afferent and efferent vagal neurons were counted in the nodose ganglion and in the dorsal motor nucleus of the vagus, respectively. After 24 weeks of diabetes, FG was retrogradely transported to more than 50% fewer afferent and efferent vagal neurons in the STZ-diabetic compared to control rats. The diabetes-induced deficit in retrograde axonal transport of FG is likely to reflect alterations in basic axonal transport mechanisms in both the afferent and efferent vagus nerve that contribute to the previously observed reductions in neurotrophin transport.
Author Keywords: Streptozotocin-induced diabetes; Vagus nerve; Nodose ganglion; Neurotrophin; Nerve growth factor; Neurotrophin-3; Axonal transport; Retrograde transport; FluoroGold
Neuroscience classification codes: Sensory systems , Somatic and visceral afferents
Article Outline
- 1. Introduction
- 2. Materials and methods
- 2.1. Animals
- 2.2. Enzyme immunoassays for NGF and NT-3
- 2.3. RT-PCR for NGF, NT-3 and neurotrophin receptor mRNAs
- 2.4. Injections of retrograde tracer, FluoroGold
- 2.5. Data analysis
- 3. Results
- 3.1. STZ-induced hyperglycemia
- 3.2. NGF and NT-3 in vagal target tissues and neurotrophin receptors in vagal ganglia
- 3.3. Retrograde transport of FG to nodose ganglion and to DMV neurons
- 4. Discussion
- 4.1. Neurotrophin levels in vagally-innervated organs of diabetic animals
- 4.2. Vagal neurotrophin receptors in diabetes
- 4.3. Decreased retrograde transport of FG in the vagus nerves of diabetic rats
- Acknowledgements
- References
*1 Disclaimer. The opinions or assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the DoD or the USUHS. The experiments reported herein were conducted according to the principles set forth in the ‘Guide for the Care and Use of Laboratory Animals’, Institute of Animal Resources, National Research Council, DHEW Pub. No. (NIH) 74-23.
Corresponding author. Tel.: +1-301-295-3238; fax: +1-301-295-3220; email: chelke@erols.com
