Kobe Journal of Medical Sciences, 1998

TI: Alterations in retrograde axonal transport in optic nerve of type I and type II diabetic rats.

AU: Zhang-L; Inoue-M; Dong-K; Yamamoto-M

AD: Department of Ophthalmology, Kobe University School of Medicine.

SO: Kobe-J-Med-Sci. 1998 Dec; 44(5-6): 205-15

ISSN: 0023-2513

PY: 1998

LA: ENGLISH

CP: JAPAN

AB: Clinical and electrophysiological examinations have yielded visual pathway function abnormalities in both humans and animal models with diabetes mellitus (DM). However, subclinical involvement of the optic nerve has not yet been fully investigated. In this study, we demonstrated the different impairments in retrograde axonal transport occurring in selective retinal ganglion cells (RGCs) of Type I and II diabetic rats. Rats were injected with streptozotocin (STZ) to induce Type I DM. The Otsuka Long-Evans Tokushima Fatty (OLETF) rats represented the Type II DM group. The STZ-induced (Type I) diabetic rats had low body weights and significant elevations in blood glucose levels compared with the age-matched control rats. On the contrary, the OLETF rats (Type II) had high body weights and significant elevations in blood glucose concentrations compared with the age-matched controls. Fluoro-Gold (FG) was injected into the bilateral dorsal lateral geniculate nucleus. Accumulation of FG in large and medium type RGCs in STZ-induced diabetic rats was significantly decreased compared with the controls. However, the accumulation of FG in RGCs of OLETF rats did not show a significant decrease compared with the controls. Our findings suggest that, within the time frame of study, retrograde axonal transport impairment of large and medium type RGCs in the STZ-induced (Type I DM) diabetic rats was greater than in the OLETF (Type II DM) diabetic rats. Impairment of retrograde axonal transport in Type I diabetes may precede or be a consequence of metabolic dysfunctions in the large and medium-sized RGCs eventually leading to optic nerve atrophy.