Peripheral axonal neuropathies are important but poorly understood causes of neuromuscular disease. Our limited understanding of the circumstances under which axons fail in neuropathies reflects an incomplete knowledge of the physiology and metabolism of normal nerves and the compensatory metabolic responses that follow nerve injury. The present studies will begin by characterizing the perfusion, glucose utilization and bioenergetic status of normal nerves. We will then assess the effects of graded ischemia on nerve metabolism, conduction, axonal transport and fiber degeneration. Finally, we will extend these studies by measuring reactive changes in perfusion and glucose metabolism that follow crush-induced Wallerian degeneration and subsequent regeneration. These investigations will allow us to better define the metabolic requirements of normal nerves and the alterations that occur after neural injury.
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