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This Article Full Text Full Text (PDF) All Versions of this Article: 95/3/1917    most recent 00637.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Allen, L. Articles by Brown, A. M. Search for Related Content PubMed PubMed Citation Articles by Allen, L. Articles by Brown, A. M.

Fructose Supports Energy Metabolism of Some, But Not All, Axons in Adult Mouse Optic Nerve

¹MRC Applied Neuroscience Group, and ²Imaging Unit, School of Biomedical Sciences, Queens Medical Centre, University of Nottingham, Nottingham, United Kingdom; ³Departments of Anesthesiology and ⁴Neurology, University of Washington School of Medicine, Seattle, Washington

Submitted 20 June 2005; accepted in final form 31 August 2005

We used transmission electron microscopy (TEM) and electrophysiological techniques to characterize the morphology and stimulus-evoked compound action potential (CAP), respectively, of the adult mouse optic nerve (MON). Electrophysiological recordings demonstrated an identical CAP profile for each MON. An initial peak, smallest in area and presumably composed of the fastest-conducting axons displayed the lowest threshold for activation as expected for large axons. The second peak, the largest, was presumably composed of axons of intermediate diameter and conduction velocity, and the third peak was composed of the slowest and presumably smallest axons. In 10 mM fructose, the first CAP peak area was reduced by 78%, but the second and third peaks were unaffected. Histological analysis revealed a cross-sectional area of 33,346 µm², containing 24,068 axons per MON. All axons were myelinated and axon diameter ranged from 0.09 to 2.58 µm, although 80 ± 6% of the axons were <0.75 µm in diameter and only 0.6 ± 0.3% of the axons were >2 µm in diameter. After bathing in fructose for 2 h 94 ± 2% of normal appearing axons were <0.75 µm in diameter and none were >1.5 µm—all of the larger axons being grossly abnormal in structure. We conclude that fructose is unable to support function of the larger axons contributing to the first CAP peak, thus enabling us to identify a distinct population of axons that contributes to that peak.