Submitted on June 20, 2005
Accepted on August 31, 2005
FRUCTOSE SUPPORTS ENERGY METABOLISM OF SOME, BUT NOT ALL, AXONS IN ADULT MOUSE OPTIC NERVE
Lynne Allen1, Susan Anderson2, Regina Wender3, Paul Meakin1, Bruce R Ransom4, David E Ray1, and Angus M Brown5*
1 MRC Applied Neuroscience Group, University of Nottingham, Nottingham, Nottinghamshire, United Kingdom
2 Imaging Unit, University of Nottingham, Nottingham, Nottinghamshire, United Kingdom
3 Anesthesiology, University of Washington, Seattle, WA, USA
4 Neurology, University of Washington, Seattle, WA, USA
5 MRC Applied Neuroscience Group, University of Nottingham, Nottingham, Nottinghamshire, United Kingdom; Neurology, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: ambrown{at}nottingham.ac.uk.
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 less than 0.75 µm in diameter, and only 0.6 ± 0.3 % of the axons were greater than 2 µm in diameter. After bathing in fructose for 2 hours 94 ± 2 % of normal appearing axons were less than 0.75 µm in diameter and none were over 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.
