@article{720d4d1f9e61481fa8a600ae4150f8b9,
title = "Orthograde and retrograde axonal transport of dopamine-β-hydroxylase in ileal mesenteric nerves of rats with chronic streptozotocin diabetes",
abstract = "Rats with chronic streptozotocin-induced diabetes develop a neuropathy involving the ileal mesenteric nerves. Distal portions of these postganglionic sympathetic axons develop markedly dilated, dopamine-β-hydroxylase (DBH)-containing dystrophic swellings. These findings led us to develop a quantitative method to examine orthograde and retrograde axonal transport of DBH in ileal mesenteric nerves. Surprisingly, no significant alteration in orthograde or retrograde axonal transport of DBH was identified.",
keywords = "Autonomic (sympathetic) neuropathy, Axonal transport, Diabetes, Dopamine-β-hydroxylase, Neuroaxonal dystrophy",
author = "Schmidt, {Robert E.} and Modert, {Christopher W.} and Grabau, {Gary G.}",
note = "Funding Information: glionic sympathetic axons of diabetic ileal mesenteric nerves 15, contrasts with the essentially normal axonal transport of DBH in the same nerves, making it unlikely that there is a generalized abnormality of axonal transport in the diabetic terminal sympathetic axon. The mechanisms of receptor-mediated endocytosis of exogenous 125I-NGF, its entry into possible terminal pools of trophic substance, and eventual access to the retrograde transport machinery may differ considerably from the molecular events involved in the metabolism and eventual reversal of orthograde DBH transport at the nerve terminal Streptozotocin was kindly provided by the Upjohn Company. This study was supported by NIH Grant AM19645, a research grant from the Juvenile Diabetes Foundation, and Research Career Development Award AM01516 to R.E.S. The excellent secretarial skills of Sandy Brickey are gratefully acknowledged.",
year = "1987",
month = jan,
day = "13",
doi = "10.1016/0006-8993(87)91173-5",
language = "English",
volume = "401",
pages = "142--146",
journal = "Brain Research",
issn = "0006-8993",
number = "1",
}