Peripheral nerve structure and function in long-term galactosemic dogs: morphometric and electron microscopic analyses

Citation
K. Sugimoto et al., Peripheral nerve structure and function in long-term galactosemic dogs: morphometric and electron microscopic analyses, ACT NEUROP, 97(4), 1999, pp. 369-376
Citations number
43
Categorie Soggetti
Neurosciences & Behavoir
Journal title
ACTA NEUROPATHOLOGICA
ISSN journal
00016322 → ACNP
Volume
97
Issue
4
Year of publication
1999
Pages
369 - 376
Database
ISI
SICI code
0001-6322(199904)97:4<369:PNSAFI>2.0.ZU;2-1
Abstract
Experimental galactosemia for activating the polyol pathway is used extensi vely to explore the pathogenesis of diabetic complications. However, despit e the presence of severe neuropathy in galactosemic rats, changes in the pe ripheral nerve have not been well established in galactosemic dogs. We ther efore conducted biochemical, electrophysiological, and morphometric studies on peripheral nervous systems (PNS) in dogs given a 30% galactose diet for 44 months. Age- and sex-matched dogs given a 30% cellulose diet were used as control. Chronic galactosemia resulted in accumulation of galactitol and decrease in myo-inositol in the sciatic nerve. Electrophysiological and te ased fiber analyses demonstrated no significant abnormalities in the ulnar and peroneal nerves in galactosemic dogs. Morphometric analyses revealed a tendency of myelinated fiber atrophy (24% reduction of average fiber size) associated with 20% decrease (P < 0.05 vs control) in mean myelinated fiber occupancy rate in the peroneal nerve in galactosemic dogs. In the anterior mesenteric ganglion, there was a slight but significant increase (8%) in m ean neuronal cell size in galactosemic dogs (P < 0.05 vs control). Electron microscopy revealed that galactosemia did not produce dystrophic and degen erative changes in the autonomic ganglion in dogs. We conclude that structu ral and functional changes in the PNS of galactosemic dogs are mild and dif ferent from those of the rat model. These findings suggest that the severit y of peripheral neuropathy induced by chronic galactosemia may be species d ependent.